subject:(Vascular smooth muscle cells)

University of New South Wales

1. Li, Yue. Novel strategies to inhibit smooth muscle cell hyperplasia and intimal thickening.

Degree: Centre for Vascular Research, 2013, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/52997 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11675/SOURCE01?view=true

► Coronary artery disease (CAD), underpinned by atherosclerosis, remains a leading cause of morbidity and mortality, particularly in the Western World. Although the advent of percutaneous… (more)

▼ Coronary artery disease (CAD), underpinned by atherosclerosis, remains a leading cause of morbidity and mortality, particularly in the Western World. Although the advent of percutaneous transluminal coronary angioplasty (PTCA) has provided a fundamental change in the treatment of CAD and drug-eluting stents (DES) have brought about marked improvement, there still remain significant challenges such as restenosis and late stent thrombosis. Coronary artery bypass grafting (CABG) has been acknowledged as the most effective way to treat CAD. However saphenous vein graft failures still present a problem due to stenosis. Vascular smooth muscle cell (VSMC) proliferation and migration is the primary driver of restenosis after percutaneous coronary interventions (PCI) and vein graft failure after CABG. Endothelial dysfunction also plays an important role in both restenosis and late thrombosis following PCI. Therefore, key to the prevention of restenosis and late stent thrombosis is to suppress SMC proliferation and migration, and to enhance re-endothelialisation. The broad aim of work in this thesis is to seek more effective strategies to inhibit SMC hyperplasia and intimal thickening while promoting re-endothelialisation.More specifically, the effects of three kinds of bio-molecules on prevention of restenosis are investigated in this thesis. Firstly, a novel “cocktail” consisting of a combination of VEGF-A, VEGF-D and cRGD, which has not been studied with SMC and EC in response to injury, is tested in a rat carotid balloon injury model. Secondly, the efficacy of the DNAzyme, Dz13, targeting c-Jun is tested in the rabbit autologous vein bypass graft model using the lipid-based transfection agent 1,2- dioleoyl-3-trimethylammonium propane (DOTAP) / 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine (DOPE). Lastly, the anti-restenotic potential of miR-191, a natural microRNA inhibitor of the immediate early gene Egr-1, is examined in the balloon-injured rat carotid artery model.The data presented in this thesis demonstrates that localised delivery of Dz13, miR191 and a novel cocktail of VEGF-A, VEGF-D and cRGD can inhibit neointima formation in animal models. According to these studies, the cocktail, Dz13 and miR191 may be useful approaches for reducing in-stent restenosis and late thrombosis. The ability of these biomolecules to be delivered at a local level makes them ideal for inclusion in stent-based strategies. Advisors/Committee Members: Khachigian, Levon, Centre for Vascular Research, Faculty of Medicine, UNSW.

Subjects/Keywords: Vascular smooth muscle cells; Neointimal hyperplasia

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APA (6^th Edition):

Li, Y. (2013). Novel strategies to inhibit smooth muscle cell hyperplasia and intimal thickening. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/52997 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11675/SOURCE01?view=true

Chicago Manual of Style (16^th Edition):

Li, Yue. “Novel strategies to inhibit smooth muscle cell hyperplasia and intimal thickening.” 2013. Doctoral Dissertation, University of New South Wales. Accessed January 17, 2021. http://handle.unsw.edu.au/1959.4/52997 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11675/SOURCE01?view=true.

MLA Handbook (7^th Edition):

Li, Yue. “Novel strategies to inhibit smooth muscle cell hyperplasia and intimal thickening.” 2013. Web. 17 Jan 2021.

Vancouver:

Li Y. Novel strategies to inhibit smooth muscle cell hyperplasia and intimal thickening. [Internet] [Doctoral dissertation]. University of New South Wales; 2013. [cited 2021 Jan 17]. Available from: http://handle.unsw.edu.au/1959.4/52997 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11675/SOURCE01?view=true.

Council of Science Editors:

Li Y. Novel strategies to inhibit smooth muscle cell hyperplasia and intimal thickening. [Doctoral Dissertation]. University of New South Wales; 2013. Available from: http://handle.unsw.edu.au/1959.4/52997 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11675/SOURCE01?view=true

University of Cambridge

2. Reinhold, Johannes. Mitochondrial function in atherosclerosis and vascular smooth muscle cells.

Degree: PhD, 2019, University of Cambridge

URL: https://doi.org/10.17863/CAM.35664 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.763838

► Atherosclerosis is the leading cause of death in the Western world. Although mitochondrial DNA (mtDNA) damage has been implicated in atherosclerosis, it is unclear whether… (more)

Subjects/Keywords: 616.1; Atherosclerosis; Mitochondria; vascular smooth muscle cells

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APA (6^th Edition):

Reinhold, J. (2019). Mitochondrial function in atherosclerosis and vascular smooth muscle cells. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.35664 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.763838

Chicago Manual of Style (16^th Edition):

Reinhold, Johannes. “Mitochondrial function in atherosclerosis and vascular smooth muscle cells.” 2019. Doctoral Dissertation, University of Cambridge. Accessed January 17, 2021. https://doi.org/10.17863/CAM.35664 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.763838.

MLA Handbook (7^th Edition):

Reinhold, Johannes. “Mitochondrial function in atherosclerosis and vascular smooth muscle cells.” 2019. Web. 17 Jan 2021.

Vancouver:

Reinhold J. Mitochondrial function in atherosclerosis and vascular smooth muscle cells. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Jan 17]. Available from: https://doi.org/10.17863/CAM.35664 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.763838.

Council of Science Editors:

Reinhold J. Mitochondrial function in atherosclerosis and vascular smooth muscle cells. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://doi.org/10.17863/CAM.35664 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.763838

University of Manchester

3. Losa Llabata, Marta. Gene regulation in embryonic development.

Degree: 2016, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:295949

► Branchial arches (BAs) are a series of transient structures that develop on the ventro-lateral surface of the head in vertebrate embryos. BAs initially appear as… (more)

▼ Branchial arches (BAs) are a series of transient structures that develop on the ventro-lateral surface of the head in vertebrate embryos. BAs initially appear as a series of similar segments; as development proceeds each BA will contribute to different structures. Here, it was investigated the transcriptional mechanisms that instruct the different fates of the BAs in development. Initially, each BA contains a blood vessel, known as aortic arch (AA) artery, that connects the dorsal aorta with the heart. Remodelling of the AAs is crucial to form the adult heart circulation. This process leads to regression of the anterior AAs, running though the first and second BAs (BA1 and BA2), and persistence of the AAs contained in more posterior BAs (PBA). To identify the mechanisms that control remodelling of the AAs, we compared the transcriptomes and epigenomic landscapes of different BAs. Using RNA-seq and H3K27Ac ChIP-seq, we uncovered the activation of a vascular smooth muscle cell (VSMC) differentiation transcriptional program exclusively in the PBAs (and not in BA1/BA2). In support of this finding, we show that VSMC differentiation occurs specifically in the PBAs, but not BA1-2 in mouse embryonic development. Despite the absence of VSMC differentiation in developing BA1-2, cells harvested from these tissues reveal a spontaneous tendency to differentiate towards VSMC fate when grown in vitro, and activate several VSMC-specific genes (Myocd, Acta2, Tagln, Jag1). Together, our results suggest that forming VSMCs is a key process for the persistence of AAs. We also showed that cells derived from all BAs have the potential to differentiate to VSMCs in vitro. However, only cells in the PBAs differentiate to VSMCs in vivo, resulting in the maintenance of posterior AAs. In this study, we also uncovered a novel transcriptional principle that specifies the fate of BA2. Using ChIP-seq, we found that binding of Meis transcription factors establish a ground pattern in the BAs. Hoxa2, which specifies BA2 identity, selects a subset of Meis-bound sites. Meis binding is strongly increased at these sites, which coincide with active enhancers, linked to genes highly expressed in the BA2 and regulated by Hoxa2. Thus, Hoxa2 modifies a ground state binding of Meis to instruct segment-specific transcriptional programs. Advisors/Committee Members: HENTGES, KATHRYN KE, Hentges, Kathryn, Bobola, Nicoletta.

Subjects/Keywords: branchial arch; neural crest cells; aortic arch; vascular smooth muscle cells

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Losa Llabata, M. (2016). Gene regulation in embryonic development. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:295949

Chicago Manual of Style (16^th Edition):

Losa Llabata, Marta. “Gene regulation in embryonic development.” 2016. Doctoral Dissertation, University of Manchester. Accessed January 17, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:295949.

MLA Handbook (7^th Edition):

Losa Llabata, Marta. “Gene regulation in embryonic development.” 2016. Web. 17 Jan 2021.

Vancouver:

Losa Llabata M. Gene regulation in embryonic development. [Internet] [Doctoral dissertation]. University of Manchester; 2016. [cited 2021 Jan 17]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:295949.

Council of Science Editors:

Losa Llabata M. Gene regulation in embryonic development. [Doctoral Dissertation]. University of Manchester; 2016. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:295949

4. Nakagaki Silva, Erick Eidy. Identification of RBPMS as a smooth muscle master splicing regulator via association of its gene with super-enhancers.

Degree: PhD, 2020, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/297676

► Alternative splicing (AS) is primarily regulated by regulatory RNA-binding proteins (RBPs). It has been suggested that a small number of master splicing regulators might control… (more)

▼ Alternative splicing (AS) is primarily regulated by regulatory RNA-binding proteins (RBPs). It has been suggested that a small number of master splicing regulators might control cell-specific programs and these regulators could be identified via the association of their genes with transcriptional super-enhancers. Using this approach, RNA Binding Protein with Multiple Splicing (RBPMS) was identified as a critical splicing regulator in vascular smooth-muscle cells (SMCs). RBPMS is strongly downregulated during SMC dedifferentiation and is responsible for nearly 20% of the AS changes during this transition as indicated by mRNA-Seq of rat PAC1 cells with RBPMS-manipulated levels. RBPMS overexpression also promoted splicing events that are usually only observed in tissue SMCs. RBPMS targeted a network of proteins involved in the cytoskeleton and cell-adhesions, machineries remodelled during the transition from contractile to motile-dedifferentiated SMCs. RBPMS directly regulated target exons with a positional bias depending upon whether acting as an activator or repressor, as indicated by RBPMS-maps, in vivo transfections with minigene reporters, RBPMS RNA binding mutant, MS2 artificial tethering and lastly in vitro binding assays. RBPMS controlled splicing and activity of other splicing and post-transcriptional regulators (MBNL1, MBNL2 and LSM14B) as well as the key SMC transcription factor Myocardin. Structure-function analyses revealed that the two major RBPMS isoforms (RBPMS-A and B) have differential activity, and that dimerization and RBPMS C- terminus are essential to RBPMS splicing activity. Yet, RBPMS RRM was insufficient for splicing. In fact, a core section of the C-terminus of RBPMS-B antagonized its repressor-splicing activity. Additionally, two threonine residues of RBPMS could be phosphorylated differentially modulating RBPMS isoforms activity. Therefore, this study provides the strongest evidence to date for a molecular function of RBPMS as a splicing-regulator, matching many of the expected criteria of a master regulator of AS in differentiated VSMCs.

Subjects/Keywords: RBPMS; Vascular smooth muscle cells; Alternative splicing; PAC1 cells

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nakagaki Silva, E. E. (2020). Identification of RBPMS as a smooth muscle master splicing regulator via association of its gene with super-enhancers. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/297676

Chicago Manual of Style (16^th Edition):

Nakagaki Silva, Erick Eidy. “Identification of RBPMS as a smooth muscle master splicing regulator via association of its gene with super-enhancers.” 2020. Doctoral Dissertation, University of Cambridge. Accessed January 17, 2021. https://www.repository.cam.ac.uk/handle/1810/297676.

MLA Handbook (7^th Edition):

Nakagaki Silva, Erick Eidy. “Identification of RBPMS as a smooth muscle master splicing regulator via association of its gene with super-enhancers.” 2020. Web. 17 Jan 2021.

Vancouver:

Nakagaki Silva EE. Identification of RBPMS as a smooth muscle master splicing regulator via association of its gene with super-enhancers. [Internet] [Doctoral dissertation]. University of Cambridge; 2020. [cited 2021 Jan 17]. Available from: https://www.repository.cam.ac.uk/handle/1810/297676.

Council of Science Editors:

Nakagaki Silva EE. Identification of RBPMS as a smooth muscle master splicing regulator via association of its gene with super-enhancers. [Doctoral Dissertation]. University of Cambridge; 2020. Available from: https://www.repository.cam.ac.uk/handle/1810/297676

University of Cambridge

5. Nakagaki Silva, Erick Eidy. Identification of RBPMS as a smooth muscle master splicing regulator via association of its gene with super-enhancers.

Degree: PhD, 2019, University of Cambridge

URL: https://doi.org/10.17863/CAM.44730 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.787875

► Alternative splicing (AS) is primarily regulated by regulatory RNA-binding proteins (RBPs). It has been suggested that a small number of master splicing regulators might control… (more)

▼ Alternative splicing (AS) is primarily regulated by regulatory RNA-binding proteins (RBPs). It has been suggested that a small number of master splicing regulators might control cell-specific programs and these regulators could be identified via the association of their genes with transcriptional super-enhancers. Using this approach, RNA Binding Protein with Multiple Splicing (RBPMS) was identified as a critical splicing regulator in vascular smooth-muscle cells (SMCs). RBPMS is strongly downregulated during SMC dedifferentiation and is responsible for nearly 20% of the AS changes during this transition as indicated by mRNA-Seq of rat PAC1 cells with RBPMS-manipulated levels. RBPMS overexpression also promoted splicing events that are usually only observed in tissue SMCs. RBPMS targeted a network of proteins involved in the cytoskeleton and cell-adhesions, machineries remodelled during the transition from contractile to motile-dedifferentiated SMCs. RBPMS directly regulated target exons with a positional bias depending upon whether acting as an activator or repressor, as indicated by RBPMS-maps, in vivo transfections with minigene reporters, RBPMS RNA binding mutant, MS2 artificial tethering and lastly in vitro binding assays. RBPMS controlled splicing and activity of other splicing and post-transcriptional regulators (MBNL1, MBNL2 and LSM14B) as well as the key SMC transcription factor Myocardin. Structure-function analyses revealed that the two major RBPMS isoforms (RBPMS-A and B) have differential activity, and that dimerization and RBPMS C- terminus are essential to RBPMS splicing activity. Yet, RBPMS RRM was insufficient for splicing. In fact, a core section of the C-terminus of RBPMS-B antagonized its repressor-splicing activity. Additionally, two threonine residues of RBPMS could be phosphorylated differentially modulating RBPMS isoforms activity. Therefore, this study provides the strongest evidence to date for a molecular function of RBPMS as a splicing-regulator, matching many of the expected criteria of a master regulator of AS in differentiated VSMCs.

Subjects/Keywords: RBPMS; Vascular smooth muscle cells; Alternative splicing; PAC1 cells

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nakagaki Silva, E. E. (2019). Identification of RBPMS as a smooth muscle master splicing regulator via association of its gene with super-enhancers. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.44730 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.787875

Chicago Manual of Style (16^th Edition):

Nakagaki Silva, Erick Eidy. “Identification of RBPMS as a smooth muscle master splicing regulator via association of its gene with super-enhancers.” 2019. Doctoral Dissertation, University of Cambridge. Accessed January 17, 2021. https://doi.org/10.17863/CAM.44730 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.787875.

MLA Handbook (7^th Edition):

Nakagaki Silva, Erick Eidy. “Identification of RBPMS as a smooth muscle master splicing regulator via association of its gene with super-enhancers.” 2019. Web. 17 Jan 2021.

Vancouver:

Nakagaki Silva EE. Identification of RBPMS as a smooth muscle master splicing regulator via association of its gene with super-enhancers. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Jan 17]. Available from: https://doi.org/10.17863/CAM.44730 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.787875.

Council of Science Editors:

Nakagaki Silva EE. Identification of RBPMS as a smooth muscle master splicing regulator via association of its gene with super-enhancers. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://doi.org/10.17863/CAM.44730 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.787875

6. MATHIEU, PATTIE SMITH. Multipotent vascular stem cells and the effects of cyclic tensile strain, collagen structure and stenting on medial vascular cell populations.

Degree: School of Engineering. Discipline of Mechanical & Manuf. Eng, 2020, Trinity College Dublin

URL: http://hdl.handle.net/2262/92298

► Atherosclerosis is one of the leading causes of mortality worldwide, and presents as a narrowing or occlusion of an artery. Interventions to re-open the arterial… (more)

▼ Atherosclerosis is one of the leading causes of mortality worldwide, and presents as a narrowing or occlusion of an artery. Interventions to re-open the arterial lumen can result in re-occlusion through intimal hyperplasia. Historically only de-differentiated vascular smooth muscle cells were thought to contribute to intimal hyperplasia. However recent evidence suggests that resident medial multipotent vascular stem cells (MVSC) may also play a role. Therefore the strain response of MVSCs was investigated since these resident cells are also subjected to strain within their native environment. First, the differences between MVSC and vascular smooth muscle cell (VSMC) strain response were investigated by applying 1 Hz cyclic equiaxial strain for 24 hours, with or without TGF-?1, and evaluating the phenotypic response. In order to investigate a strain environment more similar to the one experienced in vivo, uniaxial 1Hz cyclic uniaxial tensile strain was applied at three amplitudes around a mean strain of 5%, (4-6%, 2-8% and 0-10%) for 24 or 72 hours to both cell types. The effect of extracellular matrix (ECM) was assessed by applying 0-10% 1Hz uniaxial tensile strain for 10 days. Finally, MVSC seeded on decellularized porcine carotid arteries were indented with a single wire strut either statically or dynamically to investigate MVSC response to stenting. Cells were evaluated for alignment and proliferation. In equiaxial strain experiments MVSC became more contractile when exposed to strain, while VSMC showed no phenotypic change. Under uniaxial tensile strain, both cell types exhibit strain avoidance after 24 hours. The strain avoidant response was greater for MVSC, at 24 hours while VSMC strain avoid to a greater degree after 72 hours. Both cell types also increase strain avoidance as strain amplitude is increased. MVSC and VSMC show distinct differences when strained on native ECM. Both MVSC and VSMC align parallel to the collagen fibre direction when left unstrained. When strained parallel to fibre direction, MVSC remained aligned with fibre direction, while in some cases VSMC showed strain avoidant realignment. MVSC aligned in the direction of strain showed increased proliferation, but VSMC aligned with strain showed a decreased cell number. When MVSC were tested with simulated stent strut indentation, they developed patches of dense, highly proliferative cells, mimicking what is seen in in-stent restenosis. These experiments demonstrate for the first time how the mechano-sensitivity of MVSC may play a role in in-stent restenosis. This further emphasizes the importance of strain and ECM structure in controlling the response of vascular cells in tissue engineering applications. Advisors/Committee Members: Lally, Caitriona.

Subjects/Keywords: Multipotent Vascular Stem Cells; Vascular Smooth Muscle Cells; Tensile Strain; Extracellular Matrix; In-Stent Restenosis

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APA (6^th Edition):

MATHIEU, P. S. (2020). Multipotent vascular stem cells and the effects of cyclic tensile strain, collagen structure and stenting on medial vascular cell populations. (Thesis). Trinity College Dublin. Retrieved from http://hdl.handle.net/2262/92298

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

MATHIEU, PATTIE SMITH. “Multipotent vascular stem cells and the effects of cyclic tensile strain, collagen structure and stenting on medial vascular cell populations.” 2020. Thesis, Trinity College Dublin. Accessed January 17, 2021. http://hdl.handle.net/2262/92298.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

MATHIEU, PATTIE SMITH. “Multipotent vascular stem cells and the effects of cyclic tensile strain, collagen structure and stenting on medial vascular cell populations.” 2020. Web. 17 Jan 2021.

Vancouver:

MATHIEU PS. Multipotent vascular stem cells and the effects of cyclic tensile strain, collagen structure and stenting on medial vascular cell populations. [Internet] [Thesis]. Trinity College Dublin; 2020. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/2262/92298.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

MATHIEU PS. Multipotent vascular stem cells and the effects of cyclic tensile strain, collagen structure and stenting on medial vascular cell populations. [Thesis]. Trinity College Dublin; 2020. Available from: http://hdl.handle.net/2262/92298

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Manitoba

7. Hedley, Thomas Elliot. The role of heat shock protein-60 in vascular smooth muscle cell proliferation and atherosclerotic development.

Degree: Physiology and Pathophysiology, 2017, University of Manitoba

URL: http://hdl.handle.net/1993/32376

► This study investigated whether heat shock protein-60 (Hsp60) modulates nuclear protein import (NPI) to promote vascular smooth muscle cell (VSMC) proliferation and atherosclerotic development. Rat… (more)

Subjects/Keywords: Heat shock protein-60; Atherosclerosis; Vascular smooth muscle cells

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hedley, T. E. (2017). The role of heat shock protein-60 in vascular smooth muscle cell proliferation and atherosclerotic development. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/32376

Chicago Manual of Style (16^th Edition):

Hedley, Thomas Elliot. “The role of heat shock protein-60 in vascular smooth muscle cell proliferation and atherosclerotic development.” 2017. Masters Thesis, University of Manitoba. Accessed January 17, 2021. http://hdl.handle.net/1993/32376.

MLA Handbook (7^th Edition):

Hedley, Thomas Elliot. “The role of heat shock protein-60 in vascular smooth muscle cell proliferation and atherosclerotic development.” 2017. Web. 17 Jan 2021.

Vancouver:

Hedley TE. The role of heat shock protein-60 in vascular smooth muscle cell proliferation and atherosclerotic development. [Internet] [Masters thesis]. University of Manitoba; 2017. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/1993/32376.

Council of Science Editors:

Hedley TE. The role of heat shock protein-60 in vascular smooth muscle cell proliferation and atherosclerotic development. [Masters Thesis]. University of Manitoba; 2017. Available from: http://hdl.handle.net/1993/32376

University of Cambridge

8. Dobnikar, Lina. A genome-wide, single-cell analysis of vascular smooth muscle cell plasticity.

Degree: PhD, 2020, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/301990

► Vascular smooth muscle cells (VSMCs) possess a remarkable capacity to change phenotype in response to injury or inflammation. In healthy arteries, VSMCs exist in a… (more)

▼ Vascular smooth muscle cells (VSMCs) possess a remarkable capacity to change phenotype in response to injury or inflammation. In healthy arteries, VSMCs exist in a contractile state, but upon vascular inflammation or injury, they can switch into an activated state, in which they downregulate the contractile differentiation markers and show increased migration, proliferation and secretion of proinflammatory cytokines. This process is termed phenotypic switching and can lead to VSMC accumulation within atherosclerotic plaques. Previous observations of clonal expansion of a small number of VSMCs in atherosclerosis suggested that VSMCs were functionally heterogeneous. I hypothesised that functional heterogeneity of VSMCs in disease may originate from VSMC heterogeneity in healthy arteries. In the first part of this thesis I explored the regional heterogeneity of VSMCs originating from different parts of the mouse aorta, as well as heterogeneity of VSMCs within a vascular bed using single-cell and bulk RNA sequencing. VSMCs originating from the atherosclerosis-prone aortic arch and atherosclerosis-resistant descending thoracic aorta were found to have distinct transcriptional signatures at the single-cell level. Additionally, several disease-relevant genes were observed to be heterogeneously expressed within both vascular beds. In the second chapter I identified and characterised a rare subset of VSMCs expressing Stem cell antigen 1 (SCA1). Single-cell RNA-seq was combined with VSMC-specific lineage tracing to profile gene expression in individual VSMCs from healthy mouse arteries and to compare SCA1-expressing VSMCs to other cells. SCA1-positive VSMCs were heterogeneous, with many of them expressing low levels of contractile VSMC markers. Additionally, a subset of SCA1-positive VSMCs in healthy arteries expressed transcriptional signatures characteristic of activated VSMCs involved in phenotypic switching. In the third chapter I investigated the involvement of SCA1-positive VSMCs in phenotypic switching. SCA1 upregulation was found to mark the process of VSMC phenotypic switching following in vitro culture and in vivo vascular injury. Single-cell RNA-seq profiling of VSMCs in atherosclerosis and following vascular injury showed that Ly6a/Sca1-expressing VSMCs were present and expressed transcriptional signatures similar to activated SCA1-positive cells observed in healthy arteries. Overall the results presented in this thesis highlight the heterogeneous nature of VSMCs in healthy arteries, both regionally and within a vascular bed. I identified a rare subset of SCA1-positive VSMCs with activated transcriptional signatures in healthy arteries. I hypothesised that SCA1-positive VSMCs may be responsible for clonal expansion of VSMCs in atherosclerosis, which would have clinical implications for earlier detection and specific targeting of expanding VSMCs in atherosclerosis in the future. In support of this hypothesis I have shown that Ly6a/Sca1 is upregulated in model systems of VSMC phenotypic switching and that…

Subjects/Keywords: single-cell RNA-seq; vascular smooth muscle cells; cardiovascular

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dobnikar, L. (2020). A genome-wide, single-cell analysis of vascular smooth muscle cell plasticity. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/301990

Chicago Manual of Style (16^th Edition):

Dobnikar, Lina. “A genome-wide, single-cell analysis of vascular smooth muscle cell plasticity.” 2020. Doctoral Dissertation, University of Cambridge. Accessed January 17, 2021. https://www.repository.cam.ac.uk/handle/1810/301990.

MLA Handbook (7^th Edition):

Dobnikar, Lina. “A genome-wide, single-cell analysis of vascular smooth muscle cell plasticity.” 2020. Web. 17 Jan 2021.

Vancouver:

Dobnikar L. A genome-wide, single-cell analysis of vascular smooth muscle cell plasticity. [Internet] [Doctoral dissertation]. University of Cambridge; 2020. [cited 2021 Jan 17]. Available from: https://www.repository.cam.ac.uk/handle/1810/301990.

Council of Science Editors:

Dobnikar L. A genome-wide, single-cell analysis of vascular smooth muscle cell plasticity. [Doctoral Dissertation]. University of Cambridge; 2020. Available from: https://www.repository.cam.ac.uk/handle/1810/301990

University of Minnesota

9. Steucke, Kerianne. Empirical Determination of Vascular Smooth Muscle Cell Mechano-Adaptation.

Degree: PhD, Biomedical Engineering, 2017, University of Minnesota

URL: http://hdl.handle.net/11299/201104

► Patient-specific vascular modeling seeks to provide physicians with predictive data that will enable them to make better treatment decisions and improve patient outcomes. To achieve… (more)

▼ Patient-specific vascular modeling seeks to provide physicians with predictive data that will enable them to make better treatment decisions and improve patient outcomes. To achieve this, these models must incorporate the mechanical response of the arterial components including the key mechanically active component - vascular smooth muscle cells (VSMCs). However, current models fail to incorporate the dynamic mechanically-induced VSMC growth and remodeling, or mechano-adaptation, behavior. Therefore, the focus of this work is to mathematically characterize VSMC mechano-adaptation using experimentally determined VSMC functional responses to perturbations in the surrounding mechanical environment. To test this hypothesis, we developed three experimental techniques and proposed two VSMC mechano-adaptation laws. First, we asked if vascular disease relevant changes in extracellular matrix mechanical properties would affect tissue-scale VSMC functional contractility. We adapted the muscular thin film assay to control the underlying substrate modulus and found that with increasing substrate modulus there is increasing VSMC contractility. Second, we asked if a simple growth law could capture single cell VSMC mechano-adaptation. To derive a VSMC mechano-adaptation law from experimental data, we engineered a chronic strain traction force microscopy method, which enabled us to apply a chronic step change in strain to micropatterned single VSMCs and measured their internal stress generation over time. We found that single VSMCs have a preferred homeostatic stress-state, referred to as target stress, that they return to if perturbed. This dynamic growth and remodeling response was described by a set of simple growth laws we termed a VSMC mechano-adaptation law. Finally, we elucidated the relationship between single VSMC mechano-adaptation and substrate modulus. To determine this law from experimental findings, we adapted the previous chronic strain traction force microscopy assay, such that the substrate modulus could be altered. We then tracked the temporal stress evolution of single VSMCs on three different substrate moduli and used those data to develop a substrate dependent VSMC mechano-adaptation law.

Subjects/Keywords: Biomechanics; Cardiovascular Disease; Mechano-Adaptation; Vascular Smooth Muscle Cells

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Steucke, K. (2017). Empirical Determination of Vascular Smooth Muscle Cell Mechano-Adaptation. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/201104

Chicago Manual of Style (16^th Edition):

Steucke, Kerianne. “Empirical Determination of Vascular Smooth Muscle Cell Mechano-Adaptation.” 2017. Doctoral Dissertation, University of Minnesota. Accessed January 17, 2021. http://hdl.handle.net/11299/201104.

MLA Handbook (7^th Edition):

Steucke, Kerianne. “Empirical Determination of Vascular Smooth Muscle Cell Mechano-Adaptation.” 2017. Web. 17 Jan 2021.

Vancouver:

Steucke K. Empirical Determination of Vascular Smooth Muscle Cell Mechano-Adaptation. [Internet] [Doctoral dissertation]. University of Minnesota; 2017. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/11299/201104.

Council of Science Editors:

Steucke K. Empirical Determination of Vascular Smooth Muscle Cell Mechano-Adaptation. [Doctoral Dissertation]. University of Minnesota; 2017. Available from: http://hdl.handle.net/11299/201104

Clemson University

10. Bradley, Suzanne Nicole. Stretching Vascular Smooth Muscle Cells on Micropatterned Surfaces.

Degree: MS, Bioengineering, 2018, Clemson University

URL: https://tigerprints.clemson.edu/all_theses/2957

► Vascular smooth muscle cells regulate blood flow by contracting and relaxing blood vessels. Vascular smooth muscle cells display one of two distinct phenotypes: contractile or… (more)

Subjects/Keywords: Cell Stretching; Micropatterning; Microstamping; Vascular Smooth Muscle Cells

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APA (6^th Edition):

Bradley, S. N. (2018). Stretching Vascular Smooth Muscle Cells on Micropatterned Surfaces. (Masters Thesis). Clemson University. Retrieved from https://tigerprints.clemson.edu/all_theses/2957

Chicago Manual of Style (16^th Edition):

Bradley, Suzanne Nicole. “Stretching Vascular Smooth Muscle Cells on Micropatterned Surfaces.” 2018. Masters Thesis, Clemson University. Accessed January 17, 2021. https://tigerprints.clemson.edu/all_theses/2957.

MLA Handbook (7^th Edition):

Bradley, Suzanne Nicole. “Stretching Vascular Smooth Muscle Cells on Micropatterned Surfaces.” 2018. Web. 17 Jan 2021.

Vancouver:

Bradley SN. Stretching Vascular Smooth Muscle Cells on Micropatterned Surfaces. [Internet] [Masters thesis]. Clemson University; 2018. [cited 2021 Jan 17]. Available from: https://tigerprints.clemson.edu/all_theses/2957.

Council of Science Editors:

Bradley SN. Stretching Vascular Smooth Muscle Cells on Micropatterned Surfaces. [Masters Thesis]. Clemson University; 2018. Available from: https://tigerprints.clemson.edu/all_theses/2957

University of Cambridge

11. Dobnikar, Lina. A genome-wide, single-cell analysis of vascular smooth muscle cell plasticity.

Degree: PhD, 2020, University of Cambridge

URL: https://doi.org/10.17863/CAM.49066 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.801760

► Vascular smooth muscle cells (VSMCs) possess a remarkable capacity to change phenotype in response to injury or inflammation. In healthy arteries, VSMCs exist in a… (more)

▼ Vascular smooth muscle cells (VSMCs) possess a remarkable capacity to change phenotype in response to injury or inflammation. In healthy arteries, VSMCs exist in a contractile state, but upon vascular inflammation or injury, they can switch into an activated state, in which they downregulate the contractile differentiation markers and show increased migration, proliferation and secretion of proinflammatory cytokines. This process is termed phenotypic switching and can lead to VSMC accumulation within atherosclerotic plaques. Previous observations of clonal expansion of a small number of VSMCs in atherosclerosis suggested that VSMCs were functionally heterogeneous. I hypothesised that functional heterogeneity of VSMCs in disease may originate from VSMC heterogeneity in healthy arteries. In the first part of this thesis I explored the regional heterogeneity of VSMCs originating from different parts of the mouse aorta, as well as heterogeneity of VSMCs within a vascular bed using single-cell and bulk RNA sequencing. VSMCs originating from the atherosclerosis-prone aortic arch and atherosclerosis-resistant descending thoracic aorta were found to have distinct transcriptional signatures at the single-cell level. Additionally, several disease-relevant genes were observed to be heterogeneously expressed within both vascular beds. In the second chapter I identified and characterised a rare subset of VSMCs expressing Stem cell antigen 1 (SCA1). Single-cell RNA-seq was combined with VSMC-specific lineage tracing to profile gene expression in individual VSMCs from healthy mouse arteries and to compare SCA1-expressing VSMCs to other cells. SCA1-positive VSMCs were heterogeneous, with many of them expressing low levels of contractile VSMC markers. Additionally, a subset of SCA1-positive VSMCs in healthy arteries expressed transcriptional signatures characteristic of activated VSMCs involved in phenotypic switching. In the third chapter I investigated the involvement of SCA1-positive VSMCs in phenotypic switching. SCA1 upregulation was found to mark the process of VSMC phenotypic switching following in vitro culture and in vivo vascular injury. Single-cell RNA-seq profiling of VSMCs in atherosclerosis and following vascular injury showed that Ly6a/Sca1-expressing VSMCs were present and expressed transcriptional signatures similar to activated SCA1-positive cells observed in healthy arteries. Overall the results presented in this thesis highlight the heterogeneous nature of VSMCs in healthy arteries, both regionally and within a vascular bed. I identified a rare subset of SCA1-positive VSMCs with activated transcriptional signatures in healthy arteries. I hypothesised that SCA1-positive VSMCs may be responsible for clonal expansion of VSMCs in atherosclerosis, which would have clinical implications for earlier detection and specific targeting of expanding VSMCs in atherosclerosis in the future. In support of this hypothesis I have shown that Ly6a/Sca1 is upregulated in model systems of VSMC phenotypic switching and that…

Subjects/Keywords: single-cell RNA-seq; vascular smooth muscle cells; cardiovascular

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dobnikar, L. (2020). A genome-wide, single-cell analysis of vascular smooth muscle cell plasticity. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.49066 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.801760

Chicago Manual of Style (16^th Edition):

Dobnikar, Lina. “A genome-wide, single-cell analysis of vascular smooth muscle cell plasticity.” 2020. Doctoral Dissertation, University of Cambridge. Accessed January 17, 2021. https://doi.org/10.17863/CAM.49066 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.801760.

MLA Handbook (7^th Edition):

Dobnikar, Lina. “A genome-wide, single-cell analysis of vascular smooth muscle cell plasticity.” 2020. Web. 17 Jan 2021.

Vancouver:

Dobnikar L. A genome-wide, single-cell analysis of vascular smooth muscle cell plasticity. [Internet] [Doctoral dissertation]. University of Cambridge; 2020. [cited 2021 Jan 17]. Available from: https://doi.org/10.17863/CAM.49066 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.801760.

Council of Science Editors:

Dobnikar L. A genome-wide, single-cell analysis of vascular smooth muscle cell plasticity. [Doctoral Dissertation]. University of Cambridge; 2020. Available from: https://doi.org/10.17863/CAM.49066 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.801760

University of Sydney

12. Manuneedhi Cholan, Pradeep. TRAIL: A novel atheroprotective mechanism in the vasculature .

Degree: 2019, University of Sydney

URL: http://hdl.handle.net/2123/20949

► The vasculature is critical for the maintenance of cardiovascular homeostasis. Cardiovascular disease (CVD) is characterised by endothelial cell (EC) and vascular smooth muscle cell (VSMC)… (more)

▼ The vasculature is critical for the maintenance of cardiovascular homeostasis. Cardiovascular disease (CVD) is characterised by endothelial cell (EC) and vascular smooth muscle cell (VSMC) dysfunction, in which vascular oxidative stress is a primary cause. The mechanisms and stimuli involved in vascular dysfunction are not fully characterised. Our lab showed that TNF-related apoptosis-inducing ligand (TRAIL) is a master regulator of vascular cell function, and its deletion in Apoe-/- mice accelerated atherosclerosis and CVD. TRAIL is increasingly recognised to play a protective role in CVD, however, how it may regulate vascular function is unclear. This thesis aimed to investigate TRAIL’s protective role against oxidative stress resulting in CVDs. It studied TRAIL’s role in clinical, pre-clinical and in-vitro models. This thesis also aimed to elucidate the mechanism of action of TRAIL in vascular cells in vivo using cell-specific TRAIL knockout mouse models under normal and pathological conditions. This thesis demonstrated that: i. Circulating plasma TRAIL and oxidative stress markers are negatively correlated in patients with coronary artery disease (CAD). ii. Following high fat diet (HFD), mice lacking TRAIL had endothelial dysfunction, vascular inflammation and increased vessel permeability. iii. TRAIL protected against angiotensin II (AngII)-induced oxidative stress in vitro in ECs. TRAIL also negated AngII-induced cell processes by reducing monocyte adhesion and improving permeability in-vitro in ECs. iv. EC-specific TRAIL deleted mice challenged with an HFD, experienced high plasma cholesterol, reduced blood pressure and altered gene expression profiles for inflammatory markers compared to wild type mice. v. VSMC-specific TRAIL deleted mice challenged with an HFD, displayed altered expression of genes regulating VSMC phenotype. These mice also had an enlarged liver compared to wild type mice in response to an HFD. This thesis provided novel insight into the protective role of TRAIL against endothelial dysfunction via its ability to modulate oxidative stress. This thesis studied the mechanism of action of TRAIL in vascular cells. Thus, understanding the role TRAIL plays in normal physiology and disease, may lead to potential new therapies to improve vascular functions and CVDs.

Subjects/Keywords: TRAIL; CVD; endothelium; vascular smooth muscle cells; Angiotensin II

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APA (6^th Edition):

Manuneedhi Cholan, P. (2019). TRAIL: A novel atheroprotective mechanism in the vasculature . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/20949

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Manuneedhi Cholan, Pradeep. “TRAIL: A novel atheroprotective mechanism in the vasculature .” 2019. Thesis, University of Sydney. Accessed January 17, 2021. http://hdl.handle.net/2123/20949.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Manuneedhi Cholan, Pradeep. “TRAIL: A novel atheroprotective mechanism in the vasculature .” 2019. Web. 17 Jan 2021.

Vancouver:

Manuneedhi Cholan P. TRAIL: A novel atheroprotective mechanism in the vasculature . [Internet] [Thesis]. University of Sydney; 2019. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/2123/20949.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Manuneedhi Cholan P. TRAIL: A novel atheroprotective mechanism in the vasculature . [Thesis]. University of Sydney; 2019. Available from: http://hdl.handle.net/2123/20949

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

13. F. Elli. MOLECULAR AND CELLULAR MECHANISMS OF VASCULAR CALCIFICATION: PATHOGENESIS AND TREATMENT.

Degree: 2014, Università degli Studi di Milano

URL: http://hdl.handle.net/2434/245812

► Vascular calciﬁcation is a signiﬁcant contributor to cardiovascular risk in chronic kidney disease (CKD) patients, and its extent and severity has been correlated with mortality… (more)

▼ Vascular calciﬁcation is a signiﬁcant contributor to cardiovascular risk in chronic kidney disease (CKD) patients, and its extent and severity has been correlated with mortality in several studies. Hyperphosphatemia predisposes these patients to early and progressive vascular calcification: it appears to be involved in a number of mechanisms that trigger and promote the progression of this active and cell-mediated pathological process, in which vascular smooth muscle cells (VSMCs) residing in the tunica media of blood vessels are the main cell type actively involved. We developed an in vitro model to elucidate the molecular and cellular mechanisms involved in the pathogenesis of vascular calcification: in particular, we challenged rat VSMCs for 7-15 days with high Pi (inorganic phosphorous) with the purpose to reproduce in vitro the same pathological process that occurs in CKD patients in vivo. We investigated the high Pi-induced calcium deposition and the modulation of different cellular biological processes (apoptosis, autophagy and VSMC osteoblastic differentiation) through molecular biology, proteomic and immunohistochemistry analysis. First of all, we studied the modulation of osteonectin (SPARC), a major non collagenous protein of bone matrix that is associated, generally, with remodeling of tissues, mineralization and pathological responses to injury. Since there are controversial results regarding its role during the process of vascular calcification, we investigated osteonectin expression both in vitro and ex-vivo, and the results suggest a pro-calcifying role of this protein in the process of vascular calcification. Then, we developed an experimental strategy to delay the progression of calcium deposition in our in vitro model. We studied the potential effect of repeated and short time suspension of high Pi treatment (process that we called “Wash Out”) on the progression of calcium deposition, trying to reproduce the same temporal decrease of Pi levels that occurs in CKD patients treated with haemodialysis. Surprisingly, we discovered that it is sufficient a temporary total absence or partial decrease in Pi concentration under a so called “trigger threshold” during the process of calcification to obtain a substantial inhibition of calcium deposition. The molecular and cellular pathways involved in this protective action are apoptosis, VSMC osteoblastic differentiation and autophagy: the formers are partially inhibited, while the latter is incremented after the “Wash Out” treatment. Finally, we investigated the mechanism of action of two drugs CKD patients are treated with in the attempt to reduce hyperphosphatemia and to contrast secondary hyperparathyroidism, respectively: Lanthanum Chloride (LaCl3) and Calindol. We demonstrated that these compounds significantly delay the progression of high Pi-induced VSMC calcium deposition, but with different mechanisms of action: both of them delay VSMC osteoblastic transformation, and, in particular, lanthanum chloride preserves VSMC lineage markers expression… Advisors/Committee Members: relatore: M. G. Cozzolino, correlatore: P. Ciceri, COZZOLINO, MARIO GENNARO, COZZOLINO, MARIO GENNARO.

Subjects/Keywords: Vascular calcification, Chronic Kidney Disease, Vascular Smooth Muscle Cells; Settore MED/14 - Nefrologia

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Elli, F. (2014). MOLECULAR AND CELLULAR MECHANISMS OF VASCULAR CALCIFICATION: PATHOGENESIS AND TREATMENT. (Thesis). Università degli Studi di Milano. Retrieved from http://hdl.handle.net/2434/245812

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Elli, F.. “MOLECULAR AND CELLULAR MECHANISMS OF VASCULAR CALCIFICATION: PATHOGENESIS AND TREATMENT.” 2014. Thesis, Università degli Studi di Milano. Accessed January 17, 2021. http://hdl.handle.net/2434/245812.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Elli, F.. “MOLECULAR AND CELLULAR MECHANISMS OF VASCULAR CALCIFICATION: PATHOGENESIS AND TREATMENT.” 2014. Web. 17 Jan 2021.

Vancouver:

Elli F. MOLECULAR AND CELLULAR MECHANISMS OF VASCULAR CALCIFICATION: PATHOGENESIS AND TREATMENT. [Internet] [Thesis]. Università degli Studi di Milano; 2014. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/2434/245812.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Elli F. MOLECULAR AND CELLULAR MECHANISMS OF VASCULAR CALCIFICATION: PATHOGENESIS AND TREATMENT. [Thesis]. Università degli Studi di Milano; 2014. Available from: http://hdl.handle.net/2434/245812

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Manchester

14. Gibbons, Claire. The cytoskeletal protein adducin and its role in vascular smooth muscle.

Degree: PhD, 2012, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/the-cytoskeletal-protein-adducin-and-its-role-in-vascular-smooth-muscle(66d8e7a0-68fa-41d4-91fc-a249c9a4331e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.555573

► Actin dynamics are precisely regulated by a large number of actin binding proteins which collectively alter the rates of actin filament assembly and disassembly. Spectrin,… (more)

Subjects/Keywords: 612.7; Vascular smooth muscle; Adducin

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APA (6^th Edition):

Gibbons, C. (2012). The cytoskeletal protein adducin and its role in vascular smooth muscle. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/the-cytoskeletal-protein-adducin-and-its-role-in-vascular-smooth-muscle(66d8e7a0-68fa-41d4-91fc-a249c9a4331e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.555573

Chicago Manual of Style (16^th Edition):

Gibbons, Claire. “The cytoskeletal protein adducin and its role in vascular smooth muscle.” 2012. Doctoral Dissertation, University of Manchester. Accessed January 17, 2021. https://www.research.manchester.ac.uk/portal/en/theses/the-cytoskeletal-protein-adducin-and-its-role-in-vascular-smooth-muscle(66d8e7a0-68fa-41d4-91fc-a249c9a4331e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.555573.

MLA Handbook (7^th Edition):

Gibbons, Claire. “The cytoskeletal protein adducin and its role in vascular smooth muscle.” 2012. Web. 17 Jan 2021.

Vancouver:

Gibbons C. The cytoskeletal protein adducin and its role in vascular smooth muscle. [Internet] [Doctoral dissertation]. University of Manchester; 2012. [cited 2021 Jan 17]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-cytoskeletal-protein-adducin-and-its-role-in-vascular-smooth-muscle(66d8e7a0-68fa-41d4-91fc-a249c9a4331e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.555573.

Council of Science Editors:

Gibbons C. The cytoskeletal protein adducin and its role in vascular smooth muscle. [Doctoral Dissertation]. University of Manchester; 2012. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-cytoskeletal-protein-adducin-and-its-role-in-vascular-smooth-muscle(66d8e7a0-68fa-41d4-91fc-a249c9a4331e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.555573

University of Manchester

15. Losa Llabata, Marta. Gene regulation in embryonic development.

Degree: PhD, 2016, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/gene-regulation-in-embryonic-development(8a9efb79-1ca9-409e-89b9-9d66213e593f).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703005

► Branchial arches (BAs) are a series of transient structures that develop on the ventro-lateral surface of the head in vertebrate embryos. BAs initially appear as… (more)

▼ Branchial arches (BAs) are a series of transient structures that develop on the ventro-lateral surface of the head in vertebrate embryos. BAs initially appear as a series of similar segments; as development proceeds each BA will contribute to different structures. Here, it was investigated the transcriptional mechanisms that instruct the different fates of the BAs in development. Initially, each BA contains a blood vessel, known as aortic arch (AA) artery, that connects the dorsal aorta with the heart. Remodelling of the AAs is crucial to form the adult heart circulation. This process leads to regression of the anterior AAs, running though the first and second BAs (BA1 and BA2), and persistence of the AAs contained in more posterior BAs (PBA). To identify the mechanisms that control remodelling of the AAs, we compared the transcriptomes and epigenomic landscapes of different BAs. Using RNA-seq and H3K27Ac ChIP-seq, we uncovered the activation of a vascular smooth muscle cell (VSMC) differentiation transcriptional program exclusively in the PBAs (and not in BA1/BA2). In support of this finding, we show that VSMC differentiation occurs specifically in the PBAs, but not BA1-2 in mouse embryonic development. Despite the absence of VSMC differentiation in developing BA1-2, cells harvested from these tissues reveal a spontaneous tendency to differentiate towards VSMC fate when grown in vitro, and activate several VSMC-specific genes (Myocd, Acta2, Tagln, Jag1). Together, our results suggest that forming VSMCs is a key process for the persistence of AAs. We also showed that cells derived from all BAs have the potential to differentiate to VSMCs in vitro. However, only cells in the PBAs differentiate to VSMCs in vivo, resulting in the maintenance of posterior AAs. In this study, we also uncovered a novel transcriptional principle that specifies the fate of BA2. Using ChIP-seq, we found that binding of Meis transcription factors establish a ground pattern in the BAs. Hoxa2, which specifies BA2 identity, selects a subset of Meis-bound sites. Meis binding is strongly increased at these sites, which coincide with active enhancers, linked to genes highly expressed in the BA2 and regulated by Hoxa2. Thus, Hoxa2 modifies a ground state binding of Meis to instruct segment-specific transcriptional programs.

Subjects/Keywords: 612.6; branchial arch; neural crest cells; aortic arch; vascular smooth muscle cells

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APA (6^th Edition):

Losa Llabata, M. (2016). Gene regulation in embryonic development. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/gene-regulation-in-embryonic-development(8a9efb79-1ca9-409e-89b9-9d66213e593f).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703005

Chicago Manual of Style (16^th Edition):

Losa Llabata, Marta. “Gene regulation in embryonic development.” 2016. Doctoral Dissertation, University of Manchester. Accessed January 17, 2021. https://www.research.manchester.ac.uk/portal/en/theses/gene-regulation-in-embryonic-development(8a9efb79-1ca9-409e-89b9-9d66213e593f).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703005.

MLA Handbook (7^th Edition):

Losa Llabata, Marta. “Gene regulation in embryonic development.” 2016. Web. 17 Jan 2021.

Vancouver:

Losa Llabata M. Gene regulation in embryonic development. [Internet] [Doctoral dissertation]. University of Manchester; 2016. [cited 2021 Jan 17]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/gene-regulation-in-embryonic-development(8a9efb79-1ca9-409e-89b9-9d66213e593f).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703005.

Council of Science Editors:

Losa Llabata M. Gene regulation in embryonic development. [Doctoral Dissertation]. University of Manchester; 2016. Available from: https://www.research.manchester.ac.uk/portal/en/theses/gene-regulation-in-embryonic-development(8a9efb79-1ca9-409e-89b9-9d66213e593f).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703005

University of Vermont

16. Manuelyan, Inessa. Capsaicin-Induced Ca2+ Influx and Constriction of the Middle Meningeal Artery.

Degree: Pharmacology, 2014, University of Vermont

URL: https://scholarworks.uvm.edu/hcoltheses/200

► Research in the past on transient receptor potential cation channel subfamily V member 1 (TRPV1) has been limited to mainly nervous tissue TRPV1 because… (more)

Subjects/Keywords: Middle Meningeal Artery; Vascular Smooth Muscle TRPV1; TRPV1 mediated vasoconstriction; TRPV1 in smooth muscle cells; TRPV1-mediated mechanism of vasoconstriction

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Manuelyan, I. (2014). Capsaicin-Induced Ca2+ Influx and Constriction of the Middle Meningeal Artery. (Thesis). University of Vermont. Retrieved from https://scholarworks.uvm.edu/hcoltheses/200

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Manuelyan, Inessa. “Capsaicin-Induced Ca2+ Influx and Constriction of the Middle Meningeal Artery.” 2014. Thesis, University of Vermont. Accessed January 17, 2021. https://scholarworks.uvm.edu/hcoltheses/200.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Manuelyan, Inessa. “Capsaicin-Induced Ca2+ Influx and Constriction of the Middle Meningeal Artery.” 2014. Web. 17 Jan 2021.

Vancouver:

Manuelyan I. Capsaicin-Induced Ca2+ Influx and Constriction of the Middle Meningeal Artery. [Internet] [Thesis]. University of Vermont; 2014. [cited 2021 Jan 17]. Available from: https://scholarworks.uvm.edu/hcoltheses/200.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Manuelyan I. Capsaicin-Induced Ca2+ Influx and Constriction of the Middle Meningeal Artery. [Thesis]. University of Vermont; 2014. Available from: https://scholarworks.uvm.edu/hcoltheses/200

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Cambridge

17. Harman, Jennifer. Investigating the role of histone H3 lysine 9 dimethylation in regulating disease-associated vascular smooth muscle cell gene expression.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/289975

► Widespread changes in gene expression accompany vascular smooth muscle cell (VSMC) phenotypic switching, a hallmark of vascular disease. Upon insult, VSMCs downregulate contractile proteins and… (more)

▼ Widespread changes in gene expression accompany vascular smooth muscle cell (VSMC) phenotypic switching, a hallmark of vascular disease. Upon insult, VSMCs downregulate contractile proteins and upregulate genes linked to vascular remodelling, such as matrix metalloproteinases (MMPs) and pro-inflammatory cytokines. However, the epigenetic mechanisms which regulate VSMC phenotypic switching remain unclear. This thesis explores the role of histone 3 lysine 9 dimethylation (H3K9me2), a repressive epigenetic mark, in regulating the expression of disease-associated VSMC genes. Intriguingly, murine models of VSMC phenotypic switching revealed reduced levels of H3K9me2 upon loss of the contractile state while chromatin immunoprecipitation (ChIP) identified a subset of IL-1α/injury-responsive VSMC gene promoters enriched for H3K9me2. To test the functional importance of H3K9me2 for VSMC gene regulation the methyltransferase G9A/GLP was pharmacologically inhibited in vitro and in vivo. The resulting loss of H3K9me2 attenuated the expression of contractile VSMC markers and significantly potentiated IL-1α/injury-induced expression of MMP and pro-inflammatory genes. H3K9me2-mediated regulation of contractile and IL-1α-responsive VSMC gene expression was confirmed in cultured human VSMCs (hVSMCs). This prompted the use of hVSMCs to investigate the mechanism underlying H3K9me2-dependent regulation of IL-1α-mediated VSMC genes. Interestingly, G9A/GLP inhibition did not influence the level of IL-1α-induced nuclear localisation of the NFkB transcription factor p65 but significantly increased IL-1α-induced p65 binding to the IL6 promoter, correlating with reduced H3K9me2 levels. In contrast, enrichment of p65 was not observed at reported NFkB sites within the MMP3 promoter after IL-1α stimulation. Rather, IL-1α-induced MMP3 expression was dependent on JNK activity and G9A/GLP inhibition potentiated IL-1α-induced binding of the AP-1 transcription factor cJUN to the MMP3 promoter. Collectively, these findings suggest that H3K9me2 plays a role in maintaining the contractile VSMC state and prevents binding of both NFkB and AP-1 transcription factors at specific IL-1α-regulated genes to possibly block spurious induction of a pro-inflammatory state.

Subjects/Keywords: Vascular smooth muscle cell; H3K9me2; Vascular smooth muscle cell phenotypic switch

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Harman, J. (2019). Investigating the role of histone H3 lysine 9 dimethylation in regulating disease-associated vascular smooth muscle cell gene expression. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/289975

Chicago Manual of Style (16^th Edition):

Harman, Jennifer. “Investigating the role of histone H3 lysine 9 dimethylation in regulating disease-associated vascular smooth muscle cell gene expression.” 2019. Doctoral Dissertation, University of Cambridge. Accessed January 17, 2021. https://www.repository.cam.ac.uk/handle/1810/289975.

MLA Handbook (7^th Edition):

Harman, Jennifer. “Investigating the role of histone H3 lysine 9 dimethylation in regulating disease-associated vascular smooth muscle cell gene expression.” 2019. Web. 17 Jan 2021.

Vancouver:

Harman J. Investigating the role of histone H3 lysine 9 dimethylation in regulating disease-associated vascular smooth muscle cell gene expression. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Jan 17]. Available from: https://www.repository.cam.ac.uk/handle/1810/289975.

Council of Science Editors:

Harman J. Investigating the role of histone H3 lysine 9 dimethylation in regulating disease-associated vascular smooth muscle cell gene expression. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/289975

University of Toronto

18. Xu, Songyi. N-cadherin Regulation of Vascular Smooth Muscle Cells; the Role of DDR1 and Rho GTPases.

Degree: PhD, 2020, University of Toronto

URL: http://hdl.handle.net/1807/101328

► N-cadherin mediates cell-cell contacts in vascular smooth muscle cells (VSMCs) and regulates VSMC behaviours. Discoidin domain receptor 1 (DDR1) is a collagen binding receptor also… (more)

▼ N-cadherin mediates cell-cell contacts in vascular smooth muscle cells (VSMCs) and regulates VSMC behaviours. Discoidin domain receptor 1 (DDR1) is a collagen binding receptor also implicated in these processes. Previous studies showed that both N-cadherin and DDR1 are upregulated after vascular injury, but it is not known whether the two molecules are associated. The ability to establish proper N-cadherin junctions is important in regulating VSMC behaviour. In my studies, I found that N-cadherin could associate with DDR1, and that this association was increased during VSMC migration and wound closure. I found that N-cadherin was reduced in lipid rafts and mislocalized from cell-cell junctions in the absence of DDR1. Disruption of lipid rafts by cholesterol oxidase or methyl-β-cyclodextrin removed N-cadherin from lipid rafts of DDR1+/+ VSMCs and disrupted N-cadherin contacts, and these effects were reversed by cholesterol rescue that restored lipid rafts. Knockdown of DDR1 by siRNA resulted in mislocalized N-cadherin contacts from cell junctions, and transfection of DDR1-/- VSMCs with full-length DDR1 rescued the formation of N-cadherin junctions. The mislocalization of N-cadherin contacts in DDR1-/- VSMCs was also accompanied by disruption of the actin cytoskeleton. N-cadherin contacts in VSMCs undergo constant remodeling, especially during disease processes. Calcium switch to disrupt and restore contacts did not affect N-cadherin triton solubility in DDR1+/+ and DDR1-/- VSMCs or the association between N-cadherin and DDR1. While collagen stimulation of DDR1 increased the association between N-cadherin and DDR1 in cells with mature, well-established cell contacts, it did not affect N-cadherin localization, its triton solubility, or the association between N-cadherin and DDR1 during contact disruption, restoration, and wound closure. Rho GTPases are master regulators of the cytoskeleton and can mediate cytoskeletal processes downstream of cell-cell contacts. Using calcium switch and plating on either IgG or N-cadherin-Fc coated surfaces, active Rho GTPase pull-down assays showed a consistent decrease in Cdc42 and RhoA activity after N-cadherin contact establishment in DDR1+/+ SMCs. Overall, these data reveal that N-cadherin cell-cell contacts in VSMCs can be regulated through interaction with DDR1 and localization in lipid rafts, and that the establishment of N-cadherin contacts can suppress Rho GTPase activity. Advisors/Committee Members: Bendeck, Michelle, Laboratory Medicine and Pathobiology.

Subjects/Keywords: Cell-cell interaction; DDR1; N-cadherin; Rho GTPases; Vascular smooth muscle cells; 0307

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Xu, S. (2020). N-cadherin Regulation of Vascular Smooth Muscle Cells; the Role of DDR1 and Rho GTPases. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/101328

Chicago Manual of Style (16^th Edition):

Xu, Songyi. “N-cadherin Regulation of Vascular Smooth Muscle Cells; the Role of DDR1 and Rho GTPases.” 2020. Doctoral Dissertation, University of Toronto. Accessed January 17, 2021. http://hdl.handle.net/1807/101328.

MLA Handbook (7^th Edition):

Xu, Songyi. “N-cadherin Regulation of Vascular Smooth Muscle Cells; the Role of DDR1 and Rho GTPases.” 2020. Web. 17 Jan 2021.

Vancouver:

Xu S. N-cadherin Regulation of Vascular Smooth Muscle Cells; the Role of DDR1 and Rho GTPases. [Internet] [Doctoral dissertation]. University of Toronto; 2020. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/1807/101328.

Council of Science Editors:

Xu S. N-cadherin Regulation of Vascular Smooth Muscle Cells; the Role of DDR1 and Rho GTPases. [Doctoral Dissertation]. University of Toronto; 2020. Available from: http://hdl.handle.net/1807/101328

Delft University of Technology

19. Korevaar, Iris (author). Assesing the response of arterial and venous smooth muscle cells to varying shear stress levels.

Degree: 2019, Delft University of Technology

URL: http://resolver.tudelft.nl/uuid:66a907eb-64de-41ed-a86d-9fbae24704ca

► Worldwide 8-16% of the people are affected by chronic kidney disease (CKD). If the CKD is undetected, people have the risk to develop progressive loss… (more)

▼ Worldwide 8-16% of the people are affected by chronic kidney disease (CKD). If the CKD is undetected, people have the risk to develop progressive loss of kidney function, which can lead to kidney failure. People with kidney failure will need dialysis to take over the kidney function. For the hemodialysis a vascular access is needed, currently the preferred vascular access is an Arteriovenous fistula (AVF). But the AVF still has the limitation that maturation failure is a significant problem. The maturation failure is mainly caused by stenosis and thrombosis at the venous side of the AVF. To successfully mature the vein needs to adapt to the changes due to the creation of the AVF. Due to the higher shear stress, some of the endothelial cells in the AVF could be damaged, due to this damage arterial and venous vascular smooth muscle cells (VSMCs) are directly exposed to the blood flow. This means there will be a direct shear stress on the VSMCs. Besides this direct shear stress, venous VSMCs are also exposed to a much higher shear stress. The difference in response to this higher shear stress between the arterial and venous VSMCs may cause the problems within the AVF. In order to assess the difference in response between arterial and venous VSMCs flow experiments were performed with the IBIDI flow culturing system. HUASMCs, HUVSMCs and human primary VSMCs were used in these flow experiments. Immunofluorescence and quantitative polymerase chain reaction (qPCR) were performed to analyze the outcome of the flow experiments. This study shows that there is a difference between arterial and venous VSMCs in response to shear stress in alignment of the VSMCs after the flow experiments and within the RNA expression. But further research is necessary to confirm these findings. The results and set up of this study are a good basis for future research into the difference between arterial and venous VSMCs. Advisors/Committee Members: Zadpoor, Amir (mentor), Fratila-Apachitei, Lidy (graduation committee), Geelhoed, Wouter (graduation committee), Delft University of Technology (degree granting institution).

Subjects/Keywords: Vascular Smooth Muscle Cells; Arteriovenous fistula; Shear Stress; Flow experiments; IBIDI flow culturing system

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APA (6^th Edition):

Korevaar, I. (. (2019). Assesing the response of arterial and venous smooth muscle cells to varying shear stress levels. (Masters Thesis). Delft University of Technology. Retrieved from http://resolver.tudelft.nl/uuid:66a907eb-64de-41ed-a86d-9fbae24704ca

Chicago Manual of Style (16^th Edition):

Korevaar, Iris (author). “Assesing the response of arterial and venous smooth muscle cells to varying shear stress levels.” 2019. Masters Thesis, Delft University of Technology. Accessed January 17, 2021. http://resolver.tudelft.nl/uuid:66a907eb-64de-41ed-a86d-9fbae24704ca.

MLA Handbook (7^th Edition):

Korevaar, Iris (author). “Assesing the response of arterial and venous smooth muscle cells to varying shear stress levels.” 2019. Web. 17 Jan 2021.

Vancouver:

Korevaar I(. Assesing the response of arterial and venous smooth muscle cells to varying shear stress levels. [Internet] [Masters thesis]. Delft University of Technology; 2019. [cited 2021 Jan 17]. Available from: http://resolver.tudelft.nl/uuid:66a907eb-64de-41ed-a86d-9fbae24704ca.

Council of Science Editors:

Korevaar I(. Assesing the response of arterial and venous smooth muscle cells to varying shear stress levels. [Masters Thesis]. Delft University of Technology; 2019. Available from: http://resolver.tudelft.nl/uuid:66a907eb-64de-41ed-a86d-9fbae24704ca

Clemson University

20. Kieu, Tri. The Effects of Different Size Gold Nanoparticles on Mechanical Properties of Vascular Smooth Muscle Cells Under Mechanical Stretching.

Degree: MS, Bioengineering, 2013, Clemson University

URL: https://tigerprints.clemson.edu/all_theses/1821

► The field of nanotechnology research has seen a large growth in the past few decades due to the great potential of novel nano-size material… (more)

Subjects/Keywords: Cytotoxicity; Gold Nanoparticle; Mechanic Properties; Vascular Smooth Muscle Cells; Biomedical Engineering and Bioengineering

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kieu, T. (2013). The Effects of Different Size Gold Nanoparticles on Mechanical Properties of Vascular Smooth Muscle Cells Under Mechanical Stretching. (Masters Thesis). Clemson University. Retrieved from https://tigerprints.clemson.edu/all_theses/1821

Chicago Manual of Style (16^th Edition):

Kieu, Tri. “The Effects of Different Size Gold Nanoparticles on Mechanical Properties of Vascular Smooth Muscle Cells Under Mechanical Stretching.” 2013. Masters Thesis, Clemson University. Accessed January 17, 2021. https://tigerprints.clemson.edu/all_theses/1821.

MLA Handbook (7^th Edition):

Kieu, Tri. “The Effects of Different Size Gold Nanoparticles on Mechanical Properties of Vascular Smooth Muscle Cells Under Mechanical Stretching.” 2013. Web. 17 Jan 2021.

Vancouver:

Kieu T. The Effects of Different Size Gold Nanoparticles on Mechanical Properties of Vascular Smooth Muscle Cells Under Mechanical Stretching. [Internet] [Masters thesis]. Clemson University; 2013. [cited 2021 Jan 17]. Available from: https://tigerprints.clemson.edu/all_theses/1821.

Council of Science Editors:

Kieu T. The Effects of Different Size Gold Nanoparticles on Mechanical Properties of Vascular Smooth Muscle Cells Under Mechanical Stretching. [Masters Thesis]. Clemson University; 2013. Available from: https://tigerprints.clemson.edu/all_theses/1821

Clemson University

21. Mcallister, William. Vascular Smooth Muscle Cells in Response to Gold Nanoparticles.

Degree: MS, Bioengineering, 2011, Clemson University

URL: https://tigerprints.clemson.edu/all_theses/1101

► In this master's thesis we look at elucidating the interactions between nanoparticles and cells. Specifically, we looked at how the cell mechanics are affected, cytotoxicity… (more)

▼ In this master's thesis we look at elucidating the interactions between nanoparticles and cells. Specifically, we looked at how the cell mechanics are affected, cytotoxicity of the nanoparticles, and shifts in cell phenotypes. There has been much research looking into whether nanoparticles are cytotoxic, but limited amounts looking at their effect on mechanics especially with vascular smooth muscle cells. This cell type has two distinct phenotypes of synthetic and contractile that each serve different purposes physiologically. The first experiments we did were cytotoxicity assays to see if the cells could survive the treatment with nanoparticles. If the cells died within a short period of time then we wouldn't be able to take the next step and look at the mechanics of the cells. Most of the nanoparticles used proved to cause no change in proliferation rate of the cells; however, a couple did show some cytotoxic effects and were not used for further experimentation. Since the cells were surviving and proliferating after treatment with these nanoparticles we did atomic force microscopy to determine the elastic modulus of the cells that were treated with nanoparticles and those that were untreated. This allowed us to see if there was a significant increase or decrease caused by the nanoparticles. The results showed that there was a significant decrease in the elastic modulus of the cells treated with nanoparticles. Finally, we wanted to observe any possible phenotypic shifts in the cells by using immunofluorescence. The cells were stained for actin, microtubules (the main components of the cell's cytoskeleton and thus mechanics), and nuclei. Vascular smooth muscle cells at low passage number in culture are typically in the contractile phase and this was proven with our images. The nanoparticle treated cells showed a shift towards the synthetic phenotype which confirmed the decrease in elastic modulus from the AFM data. So, while these nanoparticles are not cytotoxic we are causing a significant change in the cells' mechanics and phenotype. Advisors/Committee Members: Dean, Delphine, Kitchens , Christopher, Alexis , Frank.

Subjects/Keywords: Atomic Force Microscopy; Cell Mechanics; Gold Nanoparticles; Vascular Smooth Muscle Cells; Biomedical Engineering and Bioengineering

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mcallister, W. (2011). Vascular Smooth Muscle Cells in Response to Gold Nanoparticles. (Masters Thesis). Clemson University. Retrieved from https://tigerprints.clemson.edu/all_theses/1101

Chicago Manual of Style (16^th Edition):

Mcallister, William. “Vascular Smooth Muscle Cells in Response to Gold Nanoparticles.” 2011. Masters Thesis, Clemson University. Accessed January 17, 2021. https://tigerprints.clemson.edu/all_theses/1101.

MLA Handbook (7^th Edition):

Mcallister, William. “Vascular Smooth Muscle Cells in Response to Gold Nanoparticles.” 2011. Web. 17 Jan 2021.

Vancouver:

Mcallister W. Vascular Smooth Muscle Cells in Response to Gold Nanoparticles. [Internet] [Masters thesis]. Clemson University; 2011. [cited 2021 Jan 17]. Available from: https://tigerprints.clemson.edu/all_theses/1101.

Council of Science Editors:

Mcallister W. Vascular Smooth Muscle Cells in Response to Gold Nanoparticles. [Masters Thesis]. Clemson University; 2011. Available from: https://tigerprints.clemson.edu/all_theses/1101

University of Georgia

22. Osman, Islam Abdelfattah Mohamed. Vasoprotective effects of pioglitazone, an insulin sensitizer.

Degree: 2017, University of Georgia

URL: http://hdl.handle.net/10724/36867

► Neointimal hyperplasia is a major event in atherosclerosis and restenosis after angioplasty. It is attributable, in part, to exaggerated proliferation of vascular smooth muscle cells… (more)

▼ Neointimal hyperplasia is a major event in atherosclerosis and restenosis after angioplasty. It is attributable, in part, to exaggerated proliferation of vascular smooth muscle cells (VSMCs). Despite the use of drug-eluting stents to limit intimal hyperplasia, in-stent restenosis still remains a major clinical problem. Several lines of evidence suggest that insulin resistance increases the risk of vascular proliferative disease. In this regard, the contribution of systemic versus vessel wall-specific insulin resistance toward dysregulated VSMC phenotype remains unclear. Pioglitazone (PIO), a classical insulin sensitizer that belongs to the family of PPARg agonists, reduces neointimal hyperplasia after coronary angioplasty in diabetic and nondiabetic subjects. However, the molecular mechanisms by which PIO regulates VSMC phenotype have not been fully elucidated. In particular, the likely intermediary role of AMP-activated protein kinase (AMPK) toward PIO inhibition of VSMC proliferation remains unclear. The objectives of our study were to examine the role of dysregulated insulin receptor signaling in VSMC proliferation and to identify the molecular mechanisms by which PIO prevents neointima formation after arterial injury. Using human aortic VSMCs in vitro, we demonstrated that high fructose treatment dysregulates proximal insulin receptor signaling events. However, high fructose did not affect platelet-derived growth factor (PDGF)-induced proliferative signaling. These findings suggest that systemic rather than VSMC-specific dysregulation of insulin signaling plays a major role in enhancing atherosclerosis and neointimal hyperplasia. Next, we demonstrated that PIO inhibits PDGF-induced key proliferative signaling events in VSMCs through AMPK-dependent and AMPK-independent mechanisms. In particular, PIO activates AMPK to induce raptor phosphorylation, which diminishes PDGF-induced mTOR activity. In addition, PIO inhibits the basal phosphorylation of ERK, independent of AMPK, thereby decreasing cyclin D1 expression and Rb phosphorylation. Furthermore, AMPK-dependent inhibition of mTOR and AMPK-independent inhibition of ERK signaling occur regardless of PPARg expression/activation in VSMCs. Using arterial injury model in vivo, we demonstrated that an AMPK inhibitor (compound C) partially reverses PIO-mediated inhibition of neointima formation. Collectively, our findings suggest that local delivery of PIO at the lesion site may limit restenosis after angioplasty without inducing PPARg- mediated systemic adverse effects

Subjects/Keywords: Arterial injury; vascular smooth muscle cells; fructose; insulin receptor signaling; pioglitazone; AMPK; p70S6K; ERK; PPARg

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APA (6^th Edition):

Osman, I. A. M. (2017). Vasoprotective effects of pioglitazone, an insulin sensitizer. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/36867

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Osman, Islam Abdelfattah Mohamed. “Vasoprotective effects of pioglitazone, an insulin sensitizer.” 2017. Thesis, University of Georgia. Accessed January 17, 2021. http://hdl.handle.net/10724/36867.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Osman, Islam Abdelfattah Mohamed. “Vasoprotective effects of pioglitazone, an insulin sensitizer.” 2017. Web. 17 Jan 2021.

Vancouver:

Osman IAM. Vasoprotective effects of pioglitazone, an insulin sensitizer. [Internet] [Thesis]. University of Georgia; 2017. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/10724/36867.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Osman IAM. Vasoprotective effects of pioglitazone, an insulin sensitizer. [Thesis]. University of Georgia; 2017. Available from: http://hdl.handle.net/10724/36867

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

23. Μίχας, Γεώργιος. Effects of glucocorticoids and of 11β - hydroxysteroid dehydrogenase type I on vascular smooth muscle cells.

Degree: 2011, University of Crete (UOC); Πανεπιστήμιο Κρήτης

URL: http://hdl.handle.net/10442/hedi/26673

► The actions of glucocorticoids are mediated, in part, by 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1), which amplifies their effects at the pre-receptor level by converting cortisone to… (more)

Subjects/Keywords: 11β - HSDI; Γλυκοκορτικοειδή; Λεία μυϊκά κύτταρα; Αγγεία; Glycocorticoids; Vascular smooth muscle cells

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APA (6^th Edition):

Μίχας, . �. (2011). Effects of glucocorticoids and of 11β - hydroxysteroid dehydrogenase type I on vascular smooth muscle cells. (Thesis). University of Crete (UOC); Πανεπιστήμιο Κρήτης. Retrieved from http://hdl.handle.net/10442/hedi/26673

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Μίχας, Γεώργιος. “Effects of glucocorticoids and of 11β - hydroxysteroid dehydrogenase type I on vascular smooth muscle cells.” 2011. Thesis, University of Crete (UOC); Πανεπιστήμιο Κρήτης. Accessed January 17, 2021. http://hdl.handle.net/10442/hedi/26673.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Μίχας, Γεώργιος. “Effects of glucocorticoids and of 11β - hydroxysteroid dehydrogenase type I on vascular smooth muscle cells.” 2011. Web. 17 Jan 2021.

Vancouver:

Μίχας �. Effects of glucocorticoids and of 11β - hydroxysteroid dehydrogenase type I on vascular smooth muscle cells. [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2011. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/10442/hedi/26673.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Μίχας �. Effects of glucocorticoids and of 11β - hydroxysteroid dehydrogenase type I on vascular smooth muscle cells. [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2011. Available from: http://hdl.handle.net/10442/hedi/26673

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

24. Zeadin, Melec. INVESTIGATING THE ROLE OF LEPTIN AND GSK-3 IN THE OSTEOGENIC DIFFERENTIATION OF VASCULAR SMOOTH MUSCLE CELLS.

Degree: PhD, 2014, McMaster University

URL: http://hdl.handle.net/11375/16509

►

Obesity is a major risk factor for insulin resistance, type 2 diabetes, cardiovascular disease (CVD), and vascular calcification. Vascular calcification is correlated with advanced CVD… (more)

▼

Obesity is a major risk factor for insulin resistance, type 2 diabetes, cardiovascular disease (CVD), and vascular calcification. Vascular calcification is correlated with advanced CVD and a significant predictor of cardiovascular events. Obese individuals tend to have increased levels of circulating leptin, an adipocytokine that is a significant independent predictor of cardiovascular disease. We have shown that daily intraperitoneal injections of exogenous leptin (125 μg/mouse/d) can promote vascular calcification in an ApoE-/- mouse model of atherosclerosis. This increase in calcification is associated with an increase in the expression of several osteoblast-specific markers and is independent of any affect on atherosclerotic lesion size. Our studies suggest that leptin mediates the osteogenic differentiation of vascular smooth muscle cells (VSMCs) to promote vascular calcification via a pathway involving the inhibition of glycogen synthase kinase (GSK)-3 activity. Other studies have suggested that endoplasmic reticulum (ER) stress-induced GSK-3 activity promotes the development of atherosclerosis. Therefore, we hypothesized that during the progression of vascular disease, GSK-3 functions as a checkpoint for VSMCs at which cells can commit to: i) de-differentiation, thereby contributing to atherosclerosis, or ii) osteogenic differentiation, thereby contributing to vascular calcification. We investigated the effects of modulating GSK-3 activity on the differentiation of VSMCs in vitro. We found that many of the molecular tools that are typically used to modulate ER stress can promote the expression of osteoblast-specific markers and the osteogenic differentiation of MOVAS cells. However, because many of these interventions affect multiple pathways in MOVAS cells, the specific role of the ER stress – GSK-3 pathway is difficult to discern. Future studies are required to determine the effects of direct modulation of GSK-3 on vascular calcification and to delineate the mechanisms/effects of various ER stressors in the osteogenic differentiation of VSMCs.

Thesis

Doctor of Philosophy (Medical Science)

Advisors/Committee Members: Werstuck, Geoff, Medical Sciences (Thrombosis & Haemostasis & Atherosclerosis).

Subjects/Keywords: leptin; vascular calcification; vascular smooth muscle cells

…90 4.3.2 Isolation of Vascular Smooth Muscle Cells… …of elastic tissue and vascular smooth muscle cells (VSMCs) which can synthesize… …Smooth Muscle Cells ................................................................ 73 3.4.5… …primary cultures of bovine aortic smooth muscle cells 10 27 Figure 1.3 Composition of GSK-3α… …Primary Cultures of Vascular Smooth Muscles Cells by Inhibiting Glycogen Synthase Kinase (…

14 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Zeadin, M. (2014). INVESTIGATING THE ROLE OF LEPTIN AND GSK-3 IN THE OSTEOGENIC DIFFERENTIATION OF VASCULAR SMOOTH MUSCLE CELLS. (Doctoral Dissertation). McMaster University. Retrieved from http://hdl.handle.net/11375/16509

Chicago Manual of Style (16^th Edition):

Zeadin, Melec. “INVESTIGATING THE ROLE OF LEPTIN AND GSK-3 IN THE OSTEOGENIC DIFFERENTIATION OF VASCULAR SMOOTH MUSCLE CELLS.” 2014. Doctoral Dissertation, McMaster University. Accessed January 17, 2021. http://hdl.handle.net/11375/16509.

MLA Handbook (7^th Edition):

Zeadin, Melec. “INVESTIGATING THE ROLE OF LEPTIN AND GSK-3 IN THE OSTEOGENIC DIFFERENTIATION OF VASCULAR SMOOTH MUSCLE CELLS.” 2014. Web. 17 Jan 2021.

Vancouver:

Zeadin M. INVESTIGATING THE ROLE OF LEPTIN AND GSK-3 IN THE OSTEOGENIC DIFFERENTIATION OF VASCULAR SMOOTH MUSCLE CELLS. [Internet] [Doctoral dissertation]. McMaster University; 2014. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/11375/16509.

Council of Science Editors:

Zeadin M. INVESTIGATING THE ROLE OF LEPTIN AND GSK-3 IN THE OSTEOGENIC DIFFERENTIATION OF VASCULAR SMOOTH MUSCLE CELLS. [Doctoral Dissertation]. McMaster University; 2014. Available from: http://hdl.handle.net/11375/16509

Boston University

25. Glazyrine, Vassili. The role of vascular endothelial growth factor in heart failure with preserved ejection fraction.

Degree: MS, Medical Sciences, 2015, Boston University

URL: http://hdl.handle.net/2144/16220

► To this day heart failure with preserved ejection fraction (HFpEF) remains a poorly understood malady. Half of all heart failure (HF) cases are HFpEF, and… (more)

▼ To this day heart failure with preserved ejection fraction (HFpEF) remains a poorly understood malady. Half of all heart failure (HF) cases are HFpEF, and the prevalence of HF is on the rise. Unlike HF with reduced ejection fraction, HFpEF has no treatment options and is often times difficult to diagnose because victims of HFpEF often have pre-existing conditions. Vascular endothelial growth factor (VEGF) has been implicated in maintaining myocardial health and is thought to play a role in HFpEF. We sought to test the hypothesis that VEGF-A plays a role in HFpEF in a hypertensive murine model of HFpEF. Using Western blot analysis we found that there was an up regulation of VEGF-A in the homogenized left ventricle (LV) of our HFpEF mice. Unexpectedly, there was a down regulation of VEGF-A in the homogenized tissue from the aorta in those mice. To study the circulating levels of VEGF in our HFpEF mice we used an ELISA. We found that our HFpEF mice had similar levels of circulating VEGF as our control. This suggests that VEGF has paracrine/autocrine role in our HFpEF model rather than endocrine, like our human data suggested. To identify the cells responsible for the expression profile we saw in the homogenized tissue data we looked at the response of adult rat ventricular myocytes (ARVM) and vascular smooth muscle cells (VSMC) to aldosterone stimulation at short (1hr) and long (24hr) time points at both physiological (50nm) and pathological (1μm) concentrations. To do this analysis we recruited the help of Western blot, ELISA and RT-PCR techniques to construct a consistent VEGF expression profile. The Western blot ARVM data showed statistically significant (P<0.05) increase in VEGF-A to pathological doses of aldosterone, especially at the longer time point. When we tested the VSMC using Western blot analysis, we found that the trend of our n=1 sample suggested a strong response to the physiological dose of aldosterone in the short term. Using the more sensitive ELISA technique to measure the VEGF content of our VCMS we increasing our sample size to n=4 and found no statistically significant (p=NS) response to aldosterone stimulation from the VSMC. However, looking at the trends in the data it is clear that VSMC increases VEGF in response to long-term physiological doses of aldosterone. This is contrary to what we found using Western blot analysis, so we queried the VEGF mRNA from the VSMC to settle the score. Unfortunately, this too proved fruitless. The RT-PCR data was not significant and the trend was that of the ARVM expression profile. We initially turned to VSMC because we hypothesized that they could contribute to the paracrine/autocrine activity similar to what we saw in the LV from the ARVM. It is unclear if VSMC play a role in HFpEF progression, but their lack of consistent response to aldosterone could potential explain the down regulation of VEGF-A we observed in the aorta of our HFpEF mice. We initially sough to test the hypothesis that VEGF-A plays a role in our HFpEF mouse model, what we found was that…

Subjects/Keywords: Medicine; HFpEF; Adult rat ventricular myocyte; Heart failure; Preserved ejection fraction; Vascular endothelial growth factor; Vascular smooth muscle cells

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Glazyrine, V. (2015). The role of vascular endothelial growth factor in heart failure with preserved ejection fraction. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/16220

Chicago Manual of Style (16^th Edition):

Glazyrine, Vassili. “The role of vascular endothelial growth factor in heart failure with preserved ejection fraction.” 2015. Masters Thesis, Boston University. Accessed January 17, 2021. http://hdl.handle.net/2144/16220.

MLA Handbook (7^th Edition):

Glazyrine, Vassili. “The role of vascular endothelial growth factor in heart failure with preserved ejection fraction.” 2015. Web. 17 Jan 2021.

Vancouver:

Glazyrine V. The role of vascular endothelial growth factor in heart failure with preserved ejection fraction. [Internet] [Masters thesis]. Boston University; 2015. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/2144/16220.

Council of Science Editors:

Glazyrine V. The role of vascular endothelial growth factor in heart failure with preserved ejection fraction. [Masters Thesis]. Boston University; 2015. Available from: http://hdl.handle.net/2144/16220

University of Washington

26. Chavkin, Nicholas Walter. Elevated Phosphate-Induced Cell Signaling through Phosphate Transporter PiT-1 in Vascular Smooth Muscle Cells.

Degree: PhD, 2017, University of Washington

URL: http://hdl.handle.net/1773/38067

► Vascular calcification (VC) is prevalent in chronic kidney disease and elevated serum inorganic phosphate (Pi) is a recognized risk factor. The type III sodium-dependent phosphate… (more)

Subjects/Keywords: Chronic Kidney Disease; Inorganic Phosphate; RapGEF1; SLC20A1; Vascular Calcification; Vascular Smooth Muscle Cells; Biomedical engineering; Cellular biology; bioengineering

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chavkin, N. W. (2017). Elevated Phosphate-Induced Cell Signaling through Phosphate Transporter PiT-1 in Vascular Smooth Muscle Cells. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/38067

Chicago Manual of Style (16^th Edition):

Chavkin, Nicholas Walter. “Elevated Phosphate-Induced Cell Signaling through Phosphate Transporter PiT-1 in Vascular Smooth Muscle Cells.” 2017. Doctoral Dissertation, University of Washington. Accessed January 17, 2021. http://hdl.handle.net/1773/38067.

MLA Handbook (7^th Edition):

Chavkin, Nicholas Walter. “Elevated Phosphate-Induced Cell Signaling through Phosphate Transporter PiT-1 in Vascular Smooth Muscle Cells.” 2017. Web. 17 Jan 2021.

Vancouver:

Chavkin NW. Elevated Phosphate-Induced Cell Signaling through Phosphate Transporter PiT-1 in Vascular Smooth Muscle Cells. [Internet] [Doctoral dissertation]. University of Washington; 2017. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/1773/38067.

Council of Science Editors:

Chavkin NW. Elevated Phosphate-Induced Cell Signaling through Phosphate Transporter PiT-1 in Vascular Smooth Muscle Cells. [Doctoral Dissertation]. University of Washington; 2017. Available from: http://hdl.handle.net/1773/38067

University of Minnesota

27. Hald, Eric. Microfabrication Approaches for Understanding the Role of Vascular Mechanics in Progressive Diseases.

Degree: PhD, Biomedical Engineering, 2016, University of Minnesota

URL: http://hdl.handle.net/11299/191352

► Vascular disease is a common cause of death that typically results from long-term alteration of vessel structure and function. The underlying mechanisms that lead to… (more)

▼ Vascular disease is a common cause of death that typically results from long-term alteration of vessel structure and function. The underlying mechanisms that lead to pathologic changes in the vasculature are largely unclear, especially in progressive diseases of the cerebral vessels. With the growing prevelance of blast traumatic brain injury in modern warfare, never before has investigation of cerebral vascular disease been more pertinent. Here, we focus on the development of microfabrication experimental approaches for probing the critical mechanical and biochemical pathways involved in progression of diseases, such as cerebral vasospasm, subarachnoid hemorrhage, and Alzheimer’s disease, that often result from TBI. First, we develop a microfluidic patterned deposition technique for studying functional mechanics in chronic vascular disease at the tissue scale. We modify substrate surfaces with genipin, a natural crosslinker, to extend culture times of in vitro vascular tissues that mimic native tissue structure and function. We successfully validate our technique, showing maintenance of patterned structural alignment and mechanical function over the course of two weeks. Lastly, we investigate the relationship between vascular disease and Alzheimer’s disease. Amyloid beta is a key precursor in the development of Alzheimer’s disease that accumulates in neuronal and cerebrovascular tissue and can result in neurodegeneration. During the development of cerebral amyloid angiopathy (CAA), which is present in over 80% of Alzheimer's disease cases, amyloid beta plaques form in the cerebral vessel walls and lead to severe attenuation of physiologic vasodilation. We measured the effect of amyloid beta treatment on vascular smooth muscle cell functional contractility using a single-cell traction force microscopy technique and developed a thin-walled arterial model for growth and remodeling response to mechanical perturbations. We found that amyloid beta induces a reduction in vascular smooth muscle cell mechanical output. We implemented this loss of function into a constrained mixture arterial model that suggests vessel growth and remodeling, in response to amyloid beta-mediated alteration of smooth muscle function, can lead to an inability of cerebral vessels to vasodilate. Our findings provide a possible explanation for the vascular injury and malfunction often associated with the development of neurodegeneration in Alzheimer’s disease.

Subjects/Keywords: Alzheimer's disease; growth and remodeling; in vitro disease model; microfabrication; vascular mechanics; vascular smooth muscle cells

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hald, E. (2016). Microfabrication Approaches for Understanding the Role of Vascular Mechanics in Progressive Diseases. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/191352

Chicago Manual of Style (16^th Edition):

Hald, Eric. “Microfabrication Approaches for Understanding the Role of Vascular Mechanics in Progressive Diseases.” 2016. Doctoral Dissertation, University of Minnesota. Accessed January 17, 2021. http://hdl.handle.net/11299/191352.

MLA Handbook (7^th Edition):

Hald, Eric. “Microfabrication Approaches for Understanding the Role of Vascular Mechanics in Progressive Diseases.” 2016. Web. 17 Jan 2021.

Vancouver:

Hald E. Microfabrication Approaches for Understanding the Role of Vascular Mechanics in Progressive Diseases. [Internet] [Doctoral dissertation]. University of Minnesota; 2016. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/11299/191352.

Council of Science Editors:

Hald E. Microfabrication Approaches for Understanding the Role of Vascular Mechanics in Progressive Diseases. [Doctoral Dissertation]. University of Minnesota; 2016. Available from: http://hdl.handle.net/11299/191352

28. Alsabeelah, Nimer Fehaid N. Vascular calcification in rat cultured smooth muscle cells : a role for nitric oxide.

Degree: PhD, 2016, University of Hertfordshire

URL: http://hdl.handle.net/2299/17217

► The underlying inflammatory storm in renal or diabetic disease may induce expression of inducible nitric oxide synthase (iNOS). Similarly, expression of iNOS or nitric oxide… (more)

▼ The underlying inflammatory storm in renal or diabetic disease may induce expression of inducible nitric oxide synthase (iNOS). Similarly, expression of iNOS or nitric oxide (NO) production in vascular smooth muscle cells (VSMCs) in a calcifying environment, may promote vascular calcification (VC) (Zaragoza et al., 2006). However, emerging data suggests that NO generated by either endothelial nitric oxide synthase (eNOS) or iNOS may protect VSMCs from VC (Kanno et al., 2008). Thus, the role of NO and its associated enzymes in the development of VC is unclear. The aim of this study was to identify whether NO produced by iNOS regulates calcification in VSMCs, and to further understanding of potential mechanisms that may mediate the actions of NO/iNOS. A significant and sustained production of NO by iNOS, which peaked at day 3 and declined thereafter was found in rat aortic smooth muscle cells (RASMCs) that were preactivated with lipopolysaccharide (LPS; 100μg ml-1) and interferon gamma (IFN-γ;100U ml-1) in the presence of calcification buffer (CB) containing calcium chloride (CaCl2; 7mM) and β-glycerophosphate (β-GP; 7mM). This was associated with formation of hydroxyapatite crystals (HA) or calcification plaques, observed via alizarin red staining (ARS) and/or fourier transform infrared (FT-IR) analysis. However, when RASMCs were incubated with the iNOS inhibitor GW274150 at 10 μM, together with LPS + IFN-γ + CB, HA crystal formation was abolished. When RASMCs were pretreated with diethylenetriamine/nitric oxide adduct (NOC 18) at either 30 or 50 μM for an hour prior to addition of CB, to generate NO; calcium levels were elevated leading to form HA crystals. However, the elevation of calcium caused by the presence of NO generated via iNOS, did not result in phosphorylation of mitogen activated protein kinases (p38 MAPK), extracellular signal-regulated kinases (Erks), and protein kinase B. Furthermore, there was a reduction of Runx2 levels (pro-calcific factor) which could be another pro-calcific factor involved in this mechanism. These findings suggest that NO may indeed play a fundamental role in calcification, enhancing mineralisation of smooth muscle cells. Furthermore, the expression of iNOS/ NO appears to be enhanced under conditions that favour calcification and these together may contribute to enhanced calcification with potential detrimental consequences in vivo.

Subjects/Keywords: 572; Vascular calcification; Nitric oxide; Inducible nitric oxide; Vascular smooth muscle cells; Runt-related transcription factor 2

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Alsabeelah, N. F. N. (2016). Vascular calcification in rat cultured smooth muscle cells : a role for nitric oxide. (Doctoral Dissertation). University of Hertfordshire. Retrieved from http://hdl.handle.net/2299/17217

Chicago Manual of Style (16^th Edition):

Alsabeelah, Nimer Fehaid N. “Vascular calcification in rat cultured smooth muscle cells : a role for nitric oxide.” 2016. Doctoral Dissertation, University of Hertfordshire. Accessed January 17, 2021. http://hdl.handle.net/2299/17217.

MLA Handbook (7^th Edition):

Alsabeelah, Nimer Fehaid N. “Vascular calcification in rat cultured smooth muscle cells : a role for nitric oxide.” 2016. Web. 17 Jan 2021.

Vancouver:

Alsabeelah NFN. Vascular calcification in rat cultured smooth muscle cells : a role for nitric oxide. [Internet] [Doctoral dissertation]. University of Hertfordshire; 2016. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/2299/17217.

Council of Science Editors:

Alsabeelah NFN. Vascular calcification in rat cultured smooth muscle cells : a role for nitric oxide. [Doctoral Dissertation]. University of Hertfordshire; 2016. Available from: http://hdl.handle.net/2299/17217

29. Padget, Rachel Lee. The Effect of Hemodynamic Force on the Maturation of Blood Vessels during Embryogenesis.

Degree: MSin Biology, Biology, 2017, Missouri State University

URL: https://bearworks.missouristate.edu/theses/3116

► Throughout embryonic development, blood vessels are derived from endothelial cells by way of vasculogenesis. During angiogenesis, vessels remodel to form a hierarchy of large-diameter… (more)

Subjects/Keywords: Vascular smooth muscle cells; vessel maturation; vascular development; angiogenesis; hemodynamic force; Biophysics; Developmental Biology; Laboratory and Basic Science Research

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Padget, R. L. (2017). The Effect of Hemodynamic Force on the Maturation of Blood Vessels during Embryogenesis. (Masters Thesis). Missouri State University. Retrieved from https://bearworks.missouristate.edu/theses/3116

Chicago Manual of Style (16^th Edition):

Padget, Rachel Lee. “The Effect of Hemodynamic Force on the Maturation of Blood Vessels during Embryogenesis.” 2017. Masters Thesis, Missouri State University. Accessed January 17, 2021. https://bearworks.missouristate.edu/theses/3116.

MLA Handbook (7^th Edition):

Padget, Rachel Lee. “The Effect of Hemodynamic Force on the Maturation of Blood Vessels during Embryogenesis.” 2017. Web. 17 Jan 2021.

Vancouver:

Padget RL. The Effect of Hemodynamic Force on the Maturation of Blood Vessels during Embryogenesis. [Internet] [Masters thesis]. Missouri State University; 2017. [cited 2021 Jan 17]. Available from: https://bearworks.missouristate.edu/theses/3116.

Council of Science Editors:

Padget RL. The Effect of Hemodynamic Force on the Maturation of Blood Vessels during Embryogenesis. [Masters Thesis]. Missouri State University; 2017. Available from: https://bearworks.missouristate.edu/theses/3116

University of Hong Kong

30. Wong, Wai-ming. Effects of isoflavonoids on vascular smooth muscle cell proliferation.

Degree: 2006, University of Hong Kong

URL: http://hdl.handle.net/10722/131317

Subjects/Keywords: Vascular smooth muscle - Cytology.; Flavonoids.; Muscle cells.

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wong, W. (2006). Effects of isoflavonoids on vascular smooth muscle cell proliferation. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/131317

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wong, Wai-ming. “Effects of isoflavonoids on vascular smooth muscle cell proliferation.” 2006. Thesis, University of Hong Kong. Accessed January 17, 2021. http://hdl.handle.net/10722/131317.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wong, Wai-ming. “Effects of isoflavonoids on vascular smooth muscle cell proliferation.” 2006. Web. 17 Jan 2021.

Vancouver:

Wong W. Effects of isoflavonoids on vascular smooth muscle cell proliferation. [Internet] [Thesis]. University of Hong Kong; 2006. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/10722/131317.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wong W. Effects of isoflavonoids on vascular smooth muscle cell proliferation. [Thesis]. University of Hong Kong; 2006. Available from: http://hdl.handle.net/10722/131317

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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