subject:(VASCULAR SMOOTH MUSCLE)

University of Manchester

1. 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)

▼ 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, an actin cross-linking protein, forms lateral filamentous networks that are linked to the plasma membrane and are required for membrane stability and resistance to mechanical stress. Adducin binds to spectrin-actin complexes, recruiting additional spectrin molecules, thereby further stabilising the membrane. In addition, adducin can bundle and cap actin filaments, and its actions have been implicated in cytoskeletal rearrangement in a variety of cell types. In vascular smooth muscle there is evidence that rearrangement of the actin cytoskeleton is involved in contraction and transmission of force to the extracellular matrix which leads to tissue remodelling. In addition, cytoskeletal dynamics are involved in vascular smooth muscle cell migration, proliferation and membrane dynamics. Protein kinase C (PKC), Rho-kinase, calmodulin and myosin light chain phosphatase are signalling proteins that are involved in these processes in vascular smooth muscle, and adducin is regulated by these signalling proteins in platelets and epithelial cells. The current study provides evidence for regulation of the actin cytoskeleton by α-adducin in vascular smooth muscle. Both α-adducin and spectrin are associated with the cytoskeleton in vascular smooth muscle cells of rat mesenteric small arteries. In response to activation by noradrenaline (NA), α-adducin becomes rapidly phosphorylated on Ser 724, a site specific for PKC, and dissociates from the actin cytoskeleton and spectrin in a PKC-dependent manner. Longer exposure of vessels to NA results in dephosphorylation of α-adducin on Ser 724 and its Rho-kinase-dependent reassociation with the actin cytoskeleton. Concurrent with this reassociation is enhanced association between the two proteins and an increase in the proportion of spectrin associated with the actin cytoskeleton. In addition, a rise in filamentous actin is observed, which can be blocked by inhibition of PKC or Rho-kinase and also by delivery of the α-adducin antibody into vessels in order to inhibit the function of endogenous a-adducin. These data provide evidence for a model in which α-adducin functions as an actin capping protein in resting vascular smooth muscle cells. Upon vasoconstrictor activation α-adducin becomes phosphorylated by PKC, inducing its dissociation from the actin cytoskeleton allowing elongation of actin filaments and further rearrangement of the actin cytoskeleton. Following this reorganisation, α-adducin re-associates with the actin cytoskeleton, possibly in response to phosphorylation by Rho-kinase, and recruits additional spectrin molecules, thus strengthening the newly formed actin filament network. These data provide further insight into the regulation of the actin cytoskeleton in vascular smooth muscle.

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 24, 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. 24 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 24]. 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 Cambridge

2. 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 (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 24, 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. 24 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 24]. 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 Vermont

3. Nystoriak, Matthew. Role of Voltage-Dependent Calcium Channels in Subarachnoid Hemorrhage-Induced Constriction of Intracerebral Arterioles.

Degree: PhD, Pharmacology, 2010, University of Vermont

URL: https://scholarworks.uvm.edu/graddis/168

► Subarachnoid hemorrhage (SAH) following cerebral aneurysm rupture is associated with substantial morbidity and mortality. The ability of SAH to induce vasospasm in large diameter pial… (more)

▼ Subarachnoid hemorrhage (SAH) following cerebral aneurysm rupture is associated with substantial morbidity and mortality. The ability of SAH to induce vasospasm in large diameter pial arteries has been extensively studied, although the contribution of this phenomenon to patient outcome is unclear. Conversely, little is known regarding the impact of SAH on intracerebral (parenchymal) arterioles, which are critical for regulation of cerebral blood flow. To assess the function of parenchymal arterioles following SAH, measurements of diameter, intracellular Ca2+ ([Ca2+]i) and membrane potential were performed in intact arterioles from unoperated (control), sham-operated and SAH model rats. At physiological intravascular pressure, parenchymal arterioles from SAH animals exhibited significantly elevated [Ca2+]i and enhanced constriction compared with arterioles from control and sham-operated animals. Elevated [Ca2+]i and enhanced tone following SAH were observed in the absence of vascular endothelium and were abolished by the L-type voltage-dependent Ca2+ channel (VDCC) inhibitor nimodipine. Molecular assessment of the L-type VDCC CaV1.2 indicated unchanged mRNA and protein expression in arterioles from SAH animals. Increased CaV1.2 activity following SAH may also reflect enhanced pressure-induced membrane potential depolarization of arteriolar smooth muscle. Membrane potential measurements in arteriolar myocytes using intracellular microelectrodes revealed approximately 7 mV depolarization at 40 mmHg in myocytes from SAH animals. Further, when membrane potential was adjusted to similar values, arteriolar [Ca2+]i and tone were similar between groups. These results demonstrate that greater pressure-dependent membrane potential depolarization results in increased activity of CaV1.2 channels, elevated [Ca2+]i and enhanced constriction of parenchymal arterioles from SAH animals. Thus, impaired regulation of parenchymal arteriolar [Ca2+]i and diameter may restrict cerebral blood flow in SAH patients. Although nimodipine is used clinically to prevent delayed neurological deficits in SAH patients, the use of this drug has been limited by hypotension and treatment options remain inadequate. Therefore, our next objective was to explore strategies to selectively suppress CaV1.2 channels in the cerebral vasculature. To do so, we examined the physiological role of smooth muscle CaV1.2 splice variants containing the alternatively-spliced exon 9* in cerebral artery constriction. Using antisense oligonucleotides, we demonstrate that suppression of exon 9*-containing CaV1.2 splice variants results in substantially reduced cerebral artery constriction to elevated extracellular [K+]. In addition, no further reduction in constriction was observed following suppression of all Cav1.2 splice variants, suggesting that exon 9* splice variants are functionally dominant in cerebral artery constriction. In summary, results shown in this dissertation demonstrate that increased CaV1.2 activity following SAH results in enhanced constriction of… Advisors/Committee Members: Wellman, George.

Subjects/Keywords: Vascular Smooth Muscle; Endothelium; Cav1.2; Artery

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

APA (6^th Edition):

Nystoriak, M. (2010). Role of Voltage-Dependent Calcium Channels in Subarachnoid Hemorrhage-Induced Constriction of Intracerebral Arterioles. (Doctoral Dissertation). University of Vermont. Retrieved from https://scholarworks.uvm.edu/graddis/168

Chicago Manual of Style (16^th Edition):

Nystoriak, Matthew. “Role of Voltage-Dependent Calcium Channels in Subarachnoid Hemorrhage-Induced Constriction of Intracerebral Arterioles.” 2010. Doctoral Dissertation, University of Vermont. Accessed January 24, 2021. https://scholarworks.uvm.edu/graddis/168.

MLA Handbook (7^th Edition):

Nystoriak, Matthew. “Role of Voltage-Dependent Calcium Channels in Subarachnoid Hemorrhage-Induced Constriction of Intracerebral Arterioles.” 2010. Web. 24 Jan 2021.

Vancouver:

Nystoriak M. Role of Voltage-Dependent Calcium Channels in Subarachnoid Hemorrhage-Induced Constriction of Intracerebral Arterioles. [Internet] [Doctoral dissertation]. University of Vermont; 2010. [cited 2021 Jan 24]. Available from: https://scholarworks.uvm.edu/graddis/168.

Council of Science Editors:

Nystoriak M. Role of Voltage-Dependent Calcium Channels in Subarachnoid Hemorrhage-Induced Constriction of Intracerebral Arterioles. [Doctoral Dissertation]. University of Vermont; 2010. Available from: https://scholarworks.uvm.edu/graddis/168

University of Aberdeen

4. Wirrig, Christiane. Effects of sphingolipids on the inflammatory reactivity of vascular smooth muscle cells.

Degree: PhD, 2012, University of Aberdeen

URL: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152414290005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558636

► Cardiovascular diseases are a major cause of death worldwide. Aneurysmal rupture in cerebral arteries or loss of endothelial integrity in the course of atherosclerosis or… (more)

▼ Cardiovascular diseases are a major cause of death worldwide. Aneurysmal rupture in cerebral arteries or loss of endothelial integrity in the course of atherosclerosis or therapeutic angioplasty lead to exposure of vascular smooth muscle cells (SMC) to blood components such as sphingolipids. Sphingosylphosphorylcholine (SPC) and sphingosine 1-phosphate (S1P) are two naturally occurring sphingolipids, which are vasoprotective in the healthy endothelium-lined vessel, but may promote vascular disease by causing functional changes of SMC. Vascular inflammation is an important factor in various pathologies. SPC can activate pro-inflammatory signalling pathways in rat cerebral artery. Here these observations are extended by showing that SPC elicits monocyte chemoattractant protein-1 production in rat cerebral artery SMC ex vivo. Thus, in addition to being a vasoconstrictor, SPC may promote the development of life-threatening prolonged cerebral vasospasm following subarachnoid haemorrhage by supporting vascular inflammation. It is also demonstrated that SPC prevents tumour necrosis factor-a (TNF)-stimulated adhesion of macrophages to rat aortic SMC in vitro by interfering with adhesive properties of SMC, but not macrophages. While this effect appeared to be mediated by the S1P receptor S1P2, S1P itself did not reduce macrophage adhesion. The anti-adhesive action of SPC also depended on lipid rafts. However, SPC did neither prevent TNF-induced nuclear factor kB activation nor cell adhesion molecule expression in SMC. SPC-induced cyclooxygenase 2 expression in aortic SMC was dispensable for its anti-adhesive effect. In contrast, the inhibitory effect of SPC on TNFinduced expression of inducible nitric oxide synthase is probably involved in its anti-adhesive effect because it was mimicked by respective pharmacological blockade. The results also demonstrate that nitric oxide promotes leukocyte adhesion to vascular SMC, while it has the opposite effect on endothelial cells. These findings may help understand cardiovascular diseases and define novel treatment approaches.

Subjects/Keywords: 616.1; Vascular smooth muscle; Sphingolipids; Atherosclerosis

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APA (6^th Edition):

Wirrig, C. (2012). Effects of sphingolipids on the inflammatory reactivity of vascular smooth muscle cells. (Doctoral Dissertation). University of Aberdeen. Retrieved from https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152414290005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558636

Chicago Manual of Style (16^th Edition):

Wirrig, Christiane. “Effects of sphingolipids on the inflammatory reactivity of vascular smooth muscle cells.” 2012. Doctoral Dissertation, University of Aberdeen. Accessed January 24, 2021. https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152414290005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558636.

MLA Handbook (7^th Edition):

Wirrig, Christiane. “Effects of sphingolipids on the inflammatory reactivity of vascular smooth muscle cells.” 2012. Web. 24 Jan 2021.

Vancouver:

Wirrig C. Effects of sphingolipids on the inflammatory reactivity of vascular smooth muscle cells. [Internet] [Doctoral dissertation]. University of Aberdeen; 2012. [cited 2021 Jan 24]. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152414290005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558636.

Council of Science Editors:

Wirrig C. Effects of sphingolipids on the inflammatory reactivity of vascular smooth muscle cells. [Doctoral Dissertation]. University of Aberdeen; 2012. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152414290005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558636

University of New South Wales

5. 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 24, 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. 24 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 24]. 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

Youngstown State University

6. Reed, Andraele N. Regulation of Aortic Smooth Muscle Relaxation in Spontaneously Hypertensive Rats.

Degree: MSin Biological Sciences, Department of Biological Sciences and Chemistry, 2014, Youngstown State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ysu1407342968

► Hypertension may be caused by excessive vasoconstriction that can occur through a variety of dysfunctions in cellular mechanisms. Estrogen has been postulated to have protective… (more)

Subjects/Keywords: Biology; hypertension; estrogen; vascular smooth muscle; relaxation

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APA (6^th Edition):

Reed, A. N. (2014). Regulation of Aortic Smooth Muscle Relaxation in Spontaneously Hypertensive Rats. (Masters Thesis). Youngstown State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ysu1407342968

Chicago Manual of Style (16^th Edition):

Reed, Andraele N. “Regulation of Aortic Smooth Muscle Relaxation in Spontaneously Hypertensive Rats.” 2014. Masters Thesis, Youngstown State University. Accessed January 24, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ysu1407342968.

MLA Handbook (7^th Edition):

Reed, Andraele N. “Regulation of Aortic Smooth Muscle Relaxation in Spontaneously Hypertensive Rats.” 2014. Web. 24 Jan 2021.

Vancouver:

Reed AN. Regulation of Aortic Smooth Muscle Relaxation in Spontaneously Hypertensive Rats. [Internet] [Masters thesis]. Youngstown State University; 2014. [cited 2021 Jan 24]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ysu1407342968.

Council of Science Editors:

Reed AN. Regulation of Aortic Smooth Muscle Relaxation in Spontaneously Hypertensive Rats. [Masters Thesis]. Youngstown State University; 2014. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ysu1407342968

University of Cambridge

7. 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 24, 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. 24 Jan 2021.

Vancouver:

Reinhold J. Mitochondrial function in atherosclerosis and vascular smooth muscle cells. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Jan 24]. 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

Texas A&M University

8. Dye, Wendy Watson. Altered biomechanical properties of large arteries in muscular dystrophy.

Degree: MS, Biomedical Engineering, 2006, Texas A&M University

URL: http://hdl.handle.net/1969.1/4304

► Muscular dystrophy is a disease characterized by skeletal muscle weakness and wasting, but little is known of alterations in the vascular system that occur with… (more)

▼ Muscular dystrophy is a disease characterized by skeletal muscle weakness and wasting, but little is known of alterations in the vascular system that occur with this disease. The culprit in many muscular dystrophies is a defective dystrophin-glycoprotein complex (DGC). The DGC is a group of transmembrane proteins that connects the cytoskeleton of muscle cells to the extracellular matrix; it plays a role in mechanotransduction and the maintenance of structural integrity of these cells, and includes the proteins dystrophin and sarcoglycan-delta. The absence of these proteins results in severe muscular dystrophies in humans, and thus knockout mice lacking the genes encoding for dystrophin (mdx mice) and sarcoglycan-delta (sgcd-/- mice) were studied to detect any vascular alterations that occur as a result of a defective DGC. Acute biaxial biomechanical data were obtained through pressure-diameter and axial force-length tests on common carotid arteries of mdx, sgcd-/-, and wild-type mice in the active and passive smooth muscle state. Functional response to the vasoreactive compounds phenylephrine, carbamylcholine chloride, and sodium nitroprusside was also tested. We found significant biomechanical differences between the knockout and wild-type mouse arteries: the mdx and sgcd-/- arteries had decreased distensibilities in pressure-diameter tests, with mdx arteries also having increased circumferential stresses, and the knockout arteries generated increased axial loads and stresses in the axial force-length tests. The mdx and sgcd-/- arteries also differed from the wild-type in that their Ã¢ÂÂhomeostaticÃ¢ÂÂ axial stretch, at which the axial force remains constant upon pressurization, was significantly decreased. We conclude that the loss of DGC proteins does trigger changes in vascular smooth muscle cells or their interactions with the extracellular matrix, yet that the altered vascular system was able to adapt and function without the DGC. Knowledge of alterations to the vascular system (and adaptations to these changes) of patients with muscular dystrophy could help physicians customize their treatment to extend and enhance their lives, especially as medical advances extend the lifespan of these patients and they begin to suffer from diseases such as hypertension and atherosclerosis that affect the normal aging population. Advisors/Committee Members: Humphrey, Jay D. (advisor), Criscione, John C. (committee member), Wilson, Emily (committee member).

Subjects/Keywords: vascular smooth muscle; vascular remodeling

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APA (6^th Edition):

Dye, W. W. (2006). Altered biomechanical properties of large arteries in muscular dystrophy. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/4304

Chicago Manual of Style (16^th Edition):

Dye, Wendy Watson. “Altered biomechanical properties of large arteries in muscular dystrophy.” 2006. Masters Thesis, Texas A&M University. Accessed January 24, 2021. http://hdl.handle.net/1969.1/4304.

MLA Handbook (7^th Edition):

Dye, Wendy Watson. “Altered biomechanical properties of large arteries in muscular dystrophy.” 2006. Web. 24 Jan 2021.

Vancouver:

Dye WW. Altered biomechanical properties of large arteries in muscular dystrophy. [Internet] [Masters thesis]. Texas A&M University; 2006. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1969.1/4304.

Council of Science Editors:

Dye WW. Altered biomechanical properties of large arteries in muscular dystrophy. [Masters Thesis]. Texas A&M University; 2006. Available from: http://hdl.handle.net/1969.1/4304

Boston University

9. Pessolano, Lawrence. Serum amyloid A and toll-like receptor 2 regulate vascular smooth muscle cell cholesterol trafficking and differentiation.

Degree: PhD, Biochemistry, 2016, Boston University

URL: http://hdl.handle.net/2144/14599

► Vascular smooth muscle cells (SMCs) regulate vessel contraction but during diseases including atherosclerosis, SMCs undergo functional changes that contribute to pathology. Chronic inflammation in the… (more)

▼ Vascular smooth muscle cells (SMCs) regulate vessel contraction but during diseases including atherosclerosis, SMCs undergo functional changes that contribute to pathology. Chronic inflammation in the vasculature exacerbates disease progression. Acute phase serum amyloid A (SAA) is up-regulated during inflammation and expressed in atherosclerotic lesions. Previous work in our laboratory demonstrated that SAA activates secretory phospholipase A2 group IIA (sPLA2), whose products impact cellular cholesterol homeostasis. It was hypothesized that SAA promotes cholesterol trafficking from the plasma membrane to the endoplasmic reticulum (ER) in an sPLA2-dependent manner. SAA induced SMC cholesterol accumulation in the ER. Levels of plasma membrane cholesterol decreased, confirming that cholesterol moved from the plasma membrane to the ER. Another family member, (cytosolic phospholipase A2, group IV), was also required for SAA-induced sPLA2 activation and cholesterol mobilization. SAA activated neutral sphingomyelinase and blocking this activity inhibited cholesterol trafficking. These studies show that SAA activated sPLA2 which activated neutral sphingomyelinase. As a result, sphingomyelin was cleaved, which liberated cholesterol for movement to the ER. Additional studies demonstrated that SAA repressed expression of SMC contractile markers including Acta2 and Myh11. Toll-like receptor 2 (TLR2) is an SAA receptor implicated in atherogenesis and it was hypothesized that TLR2 plays a role in SAA-mediated phenotype/gene changes. The TLR2 ligands, FSL and Pam3CSK4, down-regulated SMC contractile marker expression. Knockdown of TLR2 demonstrated that SAA-mediated phenotype modulation was TLR2-dependent. SAA, FSL, and Pam3CSK4 also induced mRNA expression of pro-inflammatory and adhesion genes, changes inhibited by TLR2 knockdown. SAA repressed activity of the αSMA promoter, demonstrating transcriptional regulation. Myocardin, a transcription factor required to drive expression of SMC contractile genes, was down-regulated by SAA and FSL. Myocardin overexpression abrogated SAA- and FSL-mediated repression of the αSMA and SM22α promoters. These studies demonstrate that SAA promoted a phenotypic switch through activation of TLR2 and down-regulation of myocardin expression. Taken together, novel SAA- and TLR2-mediated mechanisms of cholesterol trafficking and phenotypic modulation in SMCs are shown. Importantly, this work uncovers previously unknown effects of TLR2 signaling on vascular SMCs and provides a context by which TLR2 activation and lesion-associated SAA may promote atherosclerosis.

Subjects/Keywords: Molecular biology; Atherosclerosis; Cholesterol trafficking; Smooth muscle cell; Smooth muscle cell differentiation; Vascular biology

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

APA (6^th Edition):

Pessolano, L. (2016). Serum amyloid A and toll-like receptor 2 regulate vascular smooth muscle cell cholesterol trafficking and differentiation. (Doctoral Dissertation). Boston University. Retrieved from http://hdl.handle.net/2144/14599

Chicago Manual of Style (16^th Edition):

Pessolano, Lawrence. “Serum amyloid A and toll-like receptor 2 regulate vascular smooth muscle cell cholesterol trafficking and differentiation.” 2016. Doctoral Dissertation, Boston University. Accessed January 24, 2021. http://hdl.handle.net/2144/14599.

MLA Handbook (7^th Edition):

Pessolano, Lawrence. “Serum amyloid A and toll-like receptor 2 regulate vascular smooth muscle cell cholesterol trafficking and differentiation.” 2016. Web. 24 Jan 2021.

Vancouver:

Pessolano L. Serum amyloid A and toll-like receptor 2 regulate vascular smooth muscle cell cholesterol trafficking and differentiation. [Internet] [Doctoral dissertation]. Boston University; 2016. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/2144/14599.

Council of Science Editors:

Pessolano L. Serum amyloid A and toll-like receptor 2 regulate vascular smooth muscle cell cholesterol trafficking and differentiation. [Doctoral Dissertation]. Boston University; 2016. Available from: http://hdl.handle.net/2144/14599

University of Tasmania

10. MacPherson, Ross Duncan. The effects of anaesthetics on the reactivity of vascular smooth muscle.

Degree: 1992, University of Tasmania

URL: https://eprints.utas.edu.au/20188/1/whole_MacPhersonRossDuncan1993_thesis.pdf

► This thesis examines a number of aspects of vascular smooth muscle physiology and pharmacology. The first set of experiments examines the mechanisims of the myogenic… (more)

▼ This thesis examines a number of aspects of vascular smooth muscle physiology and pharmacology. The first set of experiments examines the mechanisims of the myogenic response in the isolated pressurised rabbit ear artery preparation, an experimental model developed here in the University of Tasmania, Department of Physiology. Rabbit ear artery segments were subjected to pressure changes in the form of either rapid increases (referred to as jumps) or slow increases (ramps). The changes in diameter of vessels as they responded to these pressure alterations were recorded. These same pressure changes were performed in vessels in four settings: in vessels where the endothelium had been removed, in vessels constricted with different vasoconstrictor agents, and at different starting diameters, in vessels dilated with either acetylcholine or sodium nitroprusside, and in vessels partly dilated with the calcium channel blocking agent, nifedipine. The results demonstrated that the endothelium was not mandatory for the myogenic response, but that acetylcholine induced endotheliumderived relaxing factor release could modify the nature of the response, as could nifedipine. The nature of vasoconstriction, and degree of constriction of the vessels were not major determinants of myogenicity. The effect of the intravenous anaesthetic agent propofol on vascular smooth muscle was then examined. This relatively recently introduced drug is known to possess significant hypotensive properties, but the mechanism of this response is unclear. In a series of experiments using the rabbit ear artery preparation, it was found that apart from having a direct vasodilator effect, propofol was a powerful attenuator of myogenicity - an effect distinct from its smooth muscle relaxant properties. This may be important in explaining the drugs hypotensive effect. Lastly, a series of experiments used the experimental apparatus to examine the effects of intra-arterial drug administration of both propofol and thiopentone. Intra-arterial administration of propofol, from clinical reports does not appear to be associated with serious hazard, a finding, in part confirmed by studies performed in this series. However, intra-arterial thiopentone administration was found to result in an almost complete destruction of the vascular endotheliuman hitherto unreported event which may well explain the reasons for the widespread vascular damage and ischaemia associated with accidental intra-arterial injection.

Subjects/Keywords: Vascular smooth muscle; Vascular smooth muscle; Anesthetics

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APA (6^th Edition):

MacPherson, R. D. (1992). The effects of anaesthetics on the reactivity of vascular smooth muscle. (Thesis). University of Tasmania. Retrieved from https://eprints.utas.edu.au/20188/1/whole_MacPhersonRossDuncan1993_thesis.pdf

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):

MacPherson, Ross Duncan. “The effects of anaesthetics on the reactivity of vascular smooth muscle.” 1992. Thesis, University of Tasmania. Accessed January 24, 2021. https://eprints.utas.edu.au/20188/1/whole_MacPhersonRossDuncan1993_thesis.pdf.

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

MLA Handbook (7^th Edition):

MacPherson, Ross Duncan. “The effects of anaesthetics on the reactivity of vascular smooth muscle.” 1992. Web. 24 Jan 2021.

Vancouver:

MacPherson RD. The effects of anaesthetics on the reactivity of vascular smooth muscle. [Internet] [Thesis]. University of Tasmania; 1992. [cited 2021 Jan 24]. Available from: https://eprints.utas.edu.au/20188/1/whole_MacPhersonRossDuncan1993_thesis.pdf.

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

Council of Science Editors:

MacPherson RD. The effects of anaesthetics on the reactivity of vascular smooth muscle. [Thesis]. University of Tasmania; 1992. Available from: https://eprints.utas.edu.au/20188/1/whole_MacPhersonRossDuncan1993_thesis.pdf

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

University of Aberdeen

11. Whyte, Claire Susan. The effect of DHA and EPA on fibrosis-related factors in vascular cells.

Degree: PhD, 2009, University of Aberdeen

URL: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152337090005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499741

► Endothelial cells (ECs) and smooth muscle cell (SMC) play a key part during development of fibrosis in the intima being partly responsible for synthesis of… (more)

Subjects/Keywords: 616.1; Atherosclerosis; Vascular smooth muscle; Muscle, Smooth, Vascular

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APA (6^th Edition):

Whyte, C. S. (2009). The effect of DHA and EPA on fibrosis-related factors in vascular cells. (Doctoral Dissertation). University of Aberdeen. Retrieved from https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152337090005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499741

Chicago Manual of Style (16^th Edition):

Whyte, Claire Susan. “The effect of DHA and EPA on fibrosis-related factors in vascular cells.” 2009. Doctoral Dissertation, University of Aberdeen. Accessed January 24, 2021. https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152337090005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499741.

MLA Handbook (7^th Edition):

Whyte, Claire Susan. “The effect of DHA and EPA on fibrosis-related factors in vascular cells.” 2009. Web. 24 Jan 2021.

Vancouver:

Whyte CS. The effect of DHA and EPA on fibrosis-related factors in vascular cells. [Internet] [Doctoral dissertation]. University of Aberdeen; 2009. [cited 2021 Jan 24]. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152337090005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499741.

Council of Science Editors:

Whyte CS. The effect of DHA and EPA on fibrosis-related factors in vascular cells. [Doctoral Dissertation]. University of Aberdeen; 2009. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152337090005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499741

University of Aberdeen

12. Whyte, Claire Susan. The effect of DHA and EPA on fibrosis-related factors in vascular cells.

Degree: School of Medicine and Dentistry., 2009, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25877 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=25877&custom_att_2=simple_viewer

Subjects/Keywords: Atherosclerosis.; Vascular smooth muscle.; Muscle, Smooth, Vascular.

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

APA (6^th Edition):

Whyte, C. S. (2009). The effect of DHA and EPA on fibrosis-related factors in vascular cells. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25877 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=25877&custom_att_2=simple_viewer

Chicago Manual of Style (16^th Edition):

Whyte, Claire Susan. “The effect of DHA and EPA on fibrosis-related factors in vascular cells.” 2009. Doctoral Dissertation, University of Aberdeen. Accessed January 24, 2021. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25877 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=25877&custom_att_2=simple_viewer.

MLA Handbook (7^th Edition):

Whyte, Claire Susan. “The effect of DHA and EPA on fibrosis-related factors in vascular cells.” 2009. Web. 24 Jan 2021.

Vancouver:

Whyte CS. The effect of DHA and EPA on fibrosis-related factors in vascular cells. [Internet] [Doctoral dissertation]. University of Aberdeen; 2009. [cited 2021 Jan 24]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25877 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=25877&custom_att_2=simple_viewer.

Council of Science Editors:

Whyte CS. The effect of DHA and EPA on fibrosis-related factors in vascular cells. [Doctoral Dissertation]. University of Aberdeen; 2009. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25877 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=25877&custom_att_2=simple_viewer

University of Hong Kong

13. 劉展彤. Modulation of vascular response by equol.

Degree: 2008, University of Hong Kong

URL: http://hdl.handle.net/10722/52316

Subjects/Keywords: Metabolites.; Vascular smooth muscle.

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

APA (6^th Edition):

劉展彤. (2008). Modulation of vascular response by equol. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/52316

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

Chicago Manual of Style (16^th Edition):

劉展彤. “Modulation of vascular response by equol.” 2008. Thesis, University of Hong Kong. Accessed January 24, 2021. http://hdl.handle.net/10722/52316.

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

MLA Handbook (7^th Edition):

劉展彤. “Modulation of vascular response by equol.” 2008. Web. 24 Jan 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

劉展彤. Modulation of vascular response by equol. [Internet] [Thesis]. University of Hong Kong; 2008. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10722/52316.

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

Council of Science Editors:

劉展彤. Modulation of vascular response by equol. [Thesis]. University of Hong Kong; 2008. Available from: http://hdl.handle.net/10722/52316

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

University of Minnesota

14. Marlatt, Kara Lynn. Endothelium-independent dilation in children and adolescents.

Degree: MS, Kinesiology, 2011, University of Minnesota

URL: http://purl.umn.edu/117070

►

University of Minnesota M.S. thesis. August 2011. Major: Kinesiology. Advisor: Donald R. Dengel, Ph.D. 1 computer file (PDF); v, 44 pages.

Peak brachial artery dilation… (more)

Subjects/Keywords: Ultrasound; Nitroglycerin; Endothelium-Independent Dilation; EID; Smooth Muscle; Vascular Function; Kinesiology

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APA (6^th Edition):

Marlatt, K. L. (2011). Endothelium-independent dilation in children and adolescents. (Masters Thesis). University of Minnesota. Retrieved from http://purl.umn.edu/117070

Chicago Manual of Style (16^th Edition):

Marlatt, Kara Lynn. “Endothelium-independent dilation in children and adolescents.” 2011. Masters Thesis, University of Minnesota. Accessed January 24, 2021. http://purl.umn.edu/117070.

MLA Handbook (7^th Edition):

Marlatt, Kara Lynn. “Endothelium-independent dilation in children and adolescents.” 2011. Web. 24 Jan 2021.

Vancouver:

Marlatt KL. Endothelium-independent dilation in children and adolescents. [Internet] [Masters thesis]. University of Minnesota; 2011. [cited 2021 Jan 24]. Available from: http://purl.umn.edu/117070.

Council of Science Editors:

Marlatt KL. Endothelium-independent dilation in children and adolescents. [Masters Thesis]. University of Minnesota; 2011. Available from: http://purl.umn.edu/117070

University of Manchester

15. 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 (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 24, 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. 24 Jan 2021.

Vancouver:

Losa Llabata M. Gene regulation in embryonic development. [Internet] [Doctoral dissertation]. University of Manchester; 2016. [cited 2021 Jan 24]. 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

University of Toronto

16. Mantella, Laura-Eve. Long Non-coding RNA Fingerprint Regulated by Cyclic Mechanical Stress in Vascular Smooth Muscle Cells: Implications for Hypertension and Aortic Aneurysms.

Degree: 2016, University of Toronto

URL: http://hdl.handle.net/1807/75343

►

Long noncoding RNAs (lncRNAs) are a new class of noncoding RNA and emerging evidence suggests that they represent a cellular hub for coordination of various… (more)

Subjects/Keywords: aortic aneurysm; hypertension; mechanical stretch; vascular smooth muscle cell; 0379

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APA (6^th Edition):

Mantella, L. (2016). Long Non-coding RNA Fingerprint Regulated by Cyclic Mechanical Stress in Vascular Smooth Muscle Cells: Implications for Hypertension and Aortic Aneurysms. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/75343

Chicago Manual of Style (16^th Edition):

Mantella, Laura-Eve. “Long Non-coding RNA Fingerprint Regulated by Cyclic Mechanical Stress in Vascular Smooth Muscle Cells: Implications for Hypertension and Aortic Aneurysms.” 2016. Masters Thesis, University of Toronto. Accessed January 24, 2021. http://hdl.handle.net/1807/75343.

MLA Handbook (7^th Edition):

Mantella, Laura-Eve. “Long Non-coding RNA Fingerprint Regulated by Cyclic Mechanical Stress in Vascular Smooth Muscle Cells: Implications for Hypertension and Aortic Aneurysms.” 2016. Web. 24 Jan 2021.

Vancouver:

Mantella L. Long Non-coding RNA Fingerprint Regulated by Cyclic Mechanical Stress in Vascular Smooth Muscle Cells: Implications for Hypertension and Aortic Aneurysms. [Internet] [Masters thesis]. University of Toronto; 2016. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1807/75343.

Council of Science Editors:

Mantella L. Long Non-coding RNA Fingerprint Regulated by Cyclic Mechanical Stress in Vascular Smooth Muscle Cells: Implications for Hypertension and Aortic Aneurysms. [Masters Thesis]. University of Toronto; 2016. Available from: http://hdl.handle.net/1807/75343

Harvard University

17. Ye, Jin Cheng. Design and Assembly Considerations in the Engineering of Vascular Tissue.

Degree: PhD, Engineering and Applied Sciences, 2014, Harvard University

URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11744451

►

Native vascular tissue functions are highly dependent on structural organization at the super-cellular, cellular, and sub-cellular spatial scales. We hypothesized that the structure-function relationship of… (more)

▼

Native vascular tissue functions are highly dependent on structural organization at the super-cellular, cellular, and sub-cellular spatial scales. We hypothesized that the structure-function relationship of vascular tissues in vivo can be leveraged to engineer vascular tissues in vitro by prescribing the shape of constituent cells and their assembly into organized three-dimensional structures. To this end, we first asked if vascular smooth muscle cell shape influences cellular contractility. We engineered human vascular smooth muscle cells to assume similar shapes to those in elastic and muscular arteries and then measured their contraction while stimulating with endothelin-1. We found that vascular smooth muscle cells with elongated shapes exhibited lower contractile strength but a greater percentage increase in contraction after endothelin-1 stimulation, suggesting that elongated vascular smooth muscle cell shape endows the muscular artery with greater dynamic contractile range. Next, we sought to assemble cells into tissues by employing a three-dimensional cellular patterning strategy based on the folding of porous, thin polymer films. We assembled different three-dimensional endothelial and vascular smooth muscle organizations by patterning two-dimensional poly(lactic-co-glycolic) acid and collagen thin films with cell suspensions at prescribed locations. The films were subsequently folded following Miura-ori geometry guidelines and the matrices were embedded subcutaneously in immunodeficient mice in order to assess the vascularization of the implanted constructs. We found that spatial organization that allowed endothelial and vascular smooth muscle cells to interact adjacent to each other laterally in the same folding plane created the densest vascularized network, suggesting that three-dimensional structural organization of vascular cells can influence the formation of vascularized networks. Taken together, our result shows that functional vascular tissues in vitro can be engineered by encoding structure cues in their design and assembly.

Engineering and Applied Sciences

Advisors/Committee Members: Parker, Kevin Kit (advisor), Mooney, David (committee member), Needleman, Daniel (committee member).

Subjects/Keywords: Biomedical engineering; assembly; design; smooth muscle; tissue; vascular

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APA (6^th Edition):

Ye, J. C. (2014). Design and Assembly Considerations in the Engineering of Vascular Tissue. (Doctoral Dissertation). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:11744451

Chicago Manual of Style (16^th Edition):

Ye, Jin Cheng. “Design and Assembly Considerations in the Engineering of Vascular Tissue.” 2014. Doctoral Dissertation, Harvard University. Accessed January 24, 2021. http://nrs.harvard.edu/urn-3:HUL.InstRepos:11744451.

MLA Handbook (7^th Edition):

Ye, Jin Cheng. “Design and Assembly Considerations in the Engineering of Vascular Tissue.” 2014. Web. 24 Jan 2021.

Vancouver:

Ye JC. Design and Assembly Considerations in the Engineering of Vascular Tissue. [Internet] [Doctoral dissertation]. Harvard University; 2014. [cited 2021 Jan 24]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11744451.

Council of Science Editors:

Ye JC. Design and Assembly Considerations in the Engineering of Vascular Tissue. [Doctoral Dissertation]. Harvard University; 2014. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11744451

18. Gibbons, Claire. THE CYTOSKELETAL PROTEIN ADDUCIN AND ITS ROLE IN VASCULAR SMOOTH MUSCLE.

Degree: 2012, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:158968

► 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)

▼ 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, an actin cross-linking protein, forms lateral filamentous networks that are linked to the plasma membrane and are required for membrane stability and resistance to mechanical stress. Adducin binds to spectrin-actin complexes, recruiting additional spectrin molecules, thereby further stabilising the membrane. In addition, adducin can bundle and cap actin filaments, and its actions have been implicated in cytoskeletal rearrangement in a variety of cell types.In vascular smooth muscle there is evidence that rearrangement of the actin cytoskeleton is involved in contraction and transmission of force to the extracellular matrix which leads to tissue remodelling. In addition, cytoskeletal dynamics are involved in vascular smooth muscle cell migration, proliferation and membrane dynamics. Protein kinase C (PKC), Rho-kinase, calmodulin and myosin light chain phosphatase are signalling proteins that are involved in these processes in vascular smooth muscle, and adducin is regulated by these signalling proteins in platelets and epithelial cells.The current study provides evidence for regulation of the actin cytoskeleton by α-adducin in vascular smooth muscle. Both α-adducin and spectrin are associated with the cytoskeleton in vascular smooth muscle cells of rat mesenteric small arteries. In response to activation by noradrenaline (NA), α-adducin becomes rapidly phosphorylated on Ser 724, a site specific for PKC, and dissociates from the actin cytoskeleton and spectrin in a PKC-dependent manner. Longer exposure of vessels to NA results in dephosphorylation of α-adducin on Ser 724 and its Rho-kinase-dependent reassociation with the actin cytoskeleton. Concurrent with this reassociation is enhanced association between the two proteins and an increase in the proportion of spectrin associated with the actin cytoskeleton. In addition, a rise in filamentous actin is observed, which can be blocked by inhibition of PKC or Rho-kinase and also by delivery of the α-adducin antibody into vessels in order to inhibit the function of endogenous -adducin. These data provide evidence for a model in which α-adducin functions as an actin capping protein in resting vascular smooth muscle cells. Upon vasoconstrictor activation α-adducin becomes phosphorylated by PKC, inducing its dissociation from the actin cytoskeleton allowing elongation of actin filaments and further rearrangement of the actin cytoskeleton. Following this reorganisation, α-adducin re-associates with the actin cytoskeleton, possibly in response to phosphorylation by Rho-kinase, and recruits additional spectrin molecules, thus strengthening the newly formed actin filament network. These data provide further insight into the regulation of the actin cytoskeleton in vascular smooth muscle. Advisors/Committee Members: OHANIAN, JACQUELINE J, Ohanian, Jacqueline, Ohanian, Vasken.

Subjects/Keywords: Vascular smooth muscle; Adducin

…junctions in smooth muscle Calcium-dependent vascular smooth muscle contraction The Rho GTPase… …filaments in vascular smooth muscle cells 125 128 129 130 132 133 135 138 139 141 143 145 147… …rearrangement in a variety of cell types. In vascular smooth muscle there is evidence that… …involved in vascular smooth muscle cell migration, proliferation and membrane dynamics. Protein… …signalling proteins that are involved in these processes in vascular smooth muscle, and adducin is…

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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 http://www.manchester.ac.uk/escholar/uk-ac-man-scw:158968

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 24, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:158968.

MLA Handbook (7^th Edition):

Gibbons, Claire. “THE CYTOSKELETAL PROTEIN ADDUCIN AND ITS ROLE IN VASCULAR SMOOTH MUSCLE.” 2012. Web. 24 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 24]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:158968.

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: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:158968

Colorado State University

19. Osterlund, Kristen Leanne. Dihydrotestosterone attenuates endotoxin, cytokine, and hypoxia-induced vascular inflammation.

Degree: PhD, Biomedical Sciences, 2011, Colorado State University

URL: http://hdl.handle.net/10217/48162

► Vascular inflammation plays a key role in the etiology of cardiovascular disease, particularly stoke. Vascular inflammation is under the control of several transcription factors, including… (more)

▼ Vascular inflammation plays a key role in the etiology of cardiovascular disease, particularly stoke. Vascular inflammation is under the control of several transcription factors, including nuclear factor kappa B and hypoxia inducible factor-1 alpha (HIF-1α). Activation of these transcription factors can lead to the production of inflammatory mediators such as cyclooxygenase-2 (COX-2). COX-2 plays a role in vascular inflammation, cerebral ischemia-induced injury, and has been implicated as a source of reactive oxygen species (ROS). Inflammatory mediators, such as endotoxin or cellular breakdown products released following injury, are known to signal through the Toll-like receptor 4 (TLR4). TLR4 activation leads to NFκB activation and subsequent production of COX-2. Like COX-2, TLR4 has also been implicated in injury-induced oxidative stress and cerebral ischemia damage. Previous studies have demonstrated that gonadal steroid hormones can also modulate vascular inflammation. Both protective and detrimental effects of androgens on the cardiovascular system have been reported. Since the potent androgen receptor (AR) agonist dihydrotestosterone (DHT) can be converted to 3β-diol, an estrogen receptor (ER) β-selective agonist, I hypothesized that ERβ may mediate some of the protective effects of androgens, while the AR may mediate some of the detrimental effects. The overall goal of this dissertation was to determine the mechanisms by which androgens can influence the vascular inflammatory response under both physiological and pathophysiological conditions. The hypothesis to be tested was that DHT influences vascular inflammation under both physiological and pathophysiological conditions. In my first set of experiments, using Western blot, I found that DHT increases expression of the vascular inflammatory mediator COX-2 under physiological conditions in human coronary artery vascular smooth muscle (VSM) cells and human brain VSM cells. This effect of DHT was attenuated in the presence of the AR antagonist bicalutamide. This data indicates that the pro-inflammatory effect of DHT under normal physiological conditions is AR mediated. In my second set of experiments, I examined the effects of DHT on vascular inflammation under a variety of pathophysiological conditions. Surprisingly, I found that DHT decreased cytokine-induced COX-2 expression and oxidative stress, endotoxin-induced COX-2 and TLR4 expression in human VSM cells. Furthermore, DHT also decreased hypoxia induced HIF-1α and COX-2 expression in human brain VSM cells and rat pial arteries. Finally, I found that DHT decreased hypoxia with glucose deprivation (HGD)-induced HIF-1α, COX-2 and TLR4 expression in human brain VSM cells. DHT`s anti-inflammatory effects during cytokine or HGD-induced inflammation in human brain VSM cells were not blocked by the AR antagonist bicalutamide, indicating that they were not AR mediated. These results led me to my second hypothesis, that DHT's anti-inflammatory effects are ERβ-mediated. In my third set of… Advisors/Committee Members: Handa, Robert (advisor), Gonzales, Rayna (committee member), Amberg, Gregory (committee member), Garrity, Deborah (committee member), Tobet, Stuart (committee member).

Subjects/Keywords: vascular smooth muscle; inflammation; ischemia; androgen; estrogen receptor beta

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APA (6^th Edition):

Osterlund, K. L. (2011). Dihydrotestosterone attenuates endotoxin, cytokine, and hypoxia-induced vascular inflammation. (Doctoral Dissertation). Colorado State University. Retrieved from http://hdl.handle.net/10217/48162

Chicago Manual of Style (16^th Edition):

Osterlund, Kristen Leanne. “Dihydrotestosterone attenuates endotoxin, cytokine, and hypoxia-induced vascular inflammation.” 2011. Doctoral Dissertation, Colorado State University. Accessed January 24, 2021. http://hdl.handle.net/10217/48162.

MLA Handbook (7^th Edition):

Osterlund, Kristen Leanne. “Dihydrotestosterone attenuates endotoxin, cytokine, and hypoxia-induced vascular inflammation.” 2011. Web. 24 Jan 2021.

Vancouver:

Osterlund KL. Dihydrotestosterone attenuates endotoxin, cytokine, and hypoxia-induced vascular inflammation. [Internet] [Doctoral dissertation]. Colorado State University; 2011. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10217/48162.

Council of Science Editors:

Osterlund KL. Dihydrotestosterone attenuates endotoxin, cytokine, and hypoxia-induced vascular inflammation. [Doctoral Dissertation]. Colorado State University; 2011. Available from: http://hdl.handle.net/10217/48162

University of Toronto

20. Hui, Sonya. Calcium-sensitive Mmechanisms in Vascular Smooth Muscle Cell Cycle Progression as Targets for Therapy.

Degree: 2010, University of Toronto

URL: http://hdl.handle.net/1807/25625

►

Increased intracellular calcium (Ca2+) is required for vascular smooth muscle cell (VSMC) proliferation through mechanisms that are not well-known. Preventing calmodulin (CaM)-cyclin E interaction with… (more)

Subjects/Keywords: Calcium; Cell Cycle; Vascular smooth muscle cell; 0719

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APA (6^th Edition):

Hui, S. (2010). Calcium-sensitive Mmechanisms in Vascular Smooth Muscle Cell Cycle Progression as Targets for Therapy. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/25625

Chicago Manual of Style (16^th Edition):

Hui, Sonya. “Calcium-sensitive Mmechanisms in Vascular Smooth Muscle Cell Cycle Progression as Targets for Therapy.” 2010. Masters Thesis, University of Toronto. Accessed January 24, 2021. http://hdl.handle.net/1807/25625.

MLA Handbook (7^th Edition):

Hui, Sonya. “Calcium-sensitive Mmechanisms in Vascular Smooth Muscle Cell Cycle Progression as Targets for Therapy.” 2010. Web. 24 Jan 2021.

Vancouver:

Hui S. Calcium-sensitive Mmechanisms in Vascular Smooth Muscle Cell Cycle Progression as Targets for Therapy. [Internet] [Masters thesis]. University of Toronto; 2010. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1807/25625.

Council of Science Editors:

Hui S. Calcium-sensitive Mmechanisms in Vascular Smooth Muscle Cell Cycle Progression as Targets for Therapy. [Masters Thesis]. University of Toronto; 2010. Available from: http://hdl.handle.net/1807/25625

Boston University

21. Poythress, Ransom Harold. Focal adhesion protein dynamics and the role of endosomes in contractile, fully differentiated, vascular smooth muscle.

Degree: PhD, Biology, 2013, Boston University

URL: http://hdl.handle.net/2144/13144

► Turnover of focal adhesions (FAs) is known to be critical for cell migration and adhesion of proliferative vascular smooth muscle cells (VSMCs). However, it is… (more)

Subjects/Keywords: Molecular biology; Adhesions; Endosomes; Focal; Muscle; Smooth; Vascular

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APA (6^th Edition):

Poythress, R. H. (2013). Focal adhesion protein dynamics and the role of endosomes in contractile, fully differentiated, vascular smooth muscle. (Doctoral Dissertation). Boston University. Retrieved from http://hdl.handle.net/2144/13144

Chicago Manual of Style (16^th Edition):

Poythress, Ransom Harold. “Focal adhesion protein dynamics and the role of endosomes in contractile, fully differentiated, vascular smooth muscle.” 2013. Doctoral Dissertation, Boston University. Accessed January 24, 2021. http://hdl.handle.net/2144/13144.

MLA Handbook (7^th Edition):

Poythress, Ransom Harold. “Focal adhesion protein dynamics and the role of endosomes in contractile, fully differentiated, vascular smooth muscle.” 2013. Web. 24 Jan 2021.

Vancouver:

Poythress RH. Focal adhesion protein dynamics and the role of endosomes in contractile, fully differentiated, vascular smooth muscle. [Internet] [Doctoral dissertation]. Boston University; 2013. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/2144/13144.

Council of Science Editors:

Poythress RH. Focal adhesion protein dynamics and the role of endosomes in contractile, fully differentiated, vascular smooth muscle. [Doctoral Dissertation]. Boston University; 2013. Available from: http://hdl.handle.net/2144/13144

22. 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 (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 24, 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. 24 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 24]. 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

Boston University

23. Elavalakanar, Pavania. Bcl11b regulates arterial stiffness by regulating vascular smooth muscle contractility.

Degree: MS, Medical Sciences, 2017, Boston University

URL: http://hdl.handle.net/2144/23716

► BACKGROUND: Arterial stiffness (AS), or loss of elastic compliance of large arteries, is an independent risk factor for cardiovascular events1. A recent study demonstrated that… (more)

Subjects/Keywords: Medicine; Aorta; Bcl11b; Arterial stiffness; Vascular smooth muscle

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APA (6^th Edition):

Elavalakanar, P. (2017). Bcl11b regulates arterial stiffness by regulating vascular smooth muscle contractility. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/23716

Chicago Manual of Style (16^th Edition):

Elavalakanar, Pavania. “Bcl11b regulates arterial stiffness by regulating vascular smooth muscle contractility.” 2017. Masters Thesis, Boston University. Accessed January 24, 2021. http://hdl.handle.net/2144/23716.

MLA Handbook (7^th Edition):

Elavalakanar, Pavania. “Bcl11b regulates arterial stiffness by regulating vascular smooth muscle contractility.” 2017. Web. 24 Jan 2021.

Vancouver:

Elavalakanar P. Bcl11b regulates arterial stiffness by regulating vascular smooth muscle contractility. [Internet] [Masters thesis]. Boston University; 2017. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/2144/23716.

Council of Science Editors:

Elavalakanar P. Bcl11b regulates arterial stiffness by regulating vascular smooth muscle contractility. [Masters Thesis]. Boston University; 2017. Available from: http://hdl.handle.net/2144/23716

24. Edgington, Nicholas P. Characterization of 5-Hydroxytryptamine-Evoked Isometric Contractile Responses in Aortic Vascular Smooth Muscle in Thyropathological Rats .

Degree: 1992, Drake U

URL: http://hdl.handle.net/2092/615

► The problem, in the past, research on these sequellae of thyropathology has utilized a variety of animal models. Recently, vascular smooth muscle has increasingly been… (more)

▼ The problem, in the past, research on these sequellae of thyropathology has utilized a variety of animal models. Recently, vascular smooth muscle has increasingly been used as an effective bioassay to assess physiological function of hormones and ligands. While general effects of thyroid status are well documented, specific thyropathologic-induced changes in 5-hydroxytryptamine (serotonergic; 5-HT) receptor function mediating contraction/dilation in rat aorta have not been completely characterized. Procedure. Aortic rings from hyperthyroid (TRX),hypothyroid (PTU), and euthyroid control (CON) rats were mounted in climate controlled tissue baths and subjected to isometric contraction experiments. The endothelium was removed from some rings (denuded) while others were left intact. All rings were initially contracted with a single dose of 55 mM KCl and then relaxed to normal potassium while concomitantly measuring the time course of this relaxation. All rings were subsequently subjected to dose/response experiments with 5-HT, either in the presence or absence of ketanserin (5-HT2 antagonist) and ICS 205-930(5-UT3 antagonist). Flndings. 5-HT generated a nonsignificant trend toward increased contractile tension in TRX rats, but a significant reduction in contractile tension in rings from PTU rats. These differences were eliminated in the denuded preparations with PTU and control tensions increasing back to TRX levels. There were no differences in sensitivity to 5-HT in the intact preparations in the three thyroid groups, but an increased sensitivity was observed in the TRX denuded preparation. Ketanserin was found to completely antagonize the 5-HT2 receptor-mediated contraction. High concentrations of 5-HT in the presence of high concentrations of ICS 205-930, generated significantly attenuated contractile tension in rings from TRX rats. Conclusions. The elimination of a significant difference in the PTU and CON treatment groups in the denuded tissue as compared to the intact tissue, suggests an enhanced 5-HT-mediated release of endothelial derived relaxing factor (EDRP) in PTU rats and reduced release in TRX rats. An incre ase in sensitivity in the denuded tissues, but not in the intact tissues, suggests an enhanced responsiveness of a 5-HT receptor subtype subserving contraction. The significant effect of micromolar concentrations of ICS 205-930 suggests that an increased contractile response in the TRX group, in light of the apparent lack of 5-HT3 sites in this tissue, may be mediated, in part, by a novel serotonergic receptor mediating contraction. Alternatively, this effect may reflect activity of the ligand at 5-HT1 or 5-HT2 receptors differentially sensitized by thyropathology. These data suggest that thyropathological alterations in 5-HT1 or 5-HT2 receptor subtype-mediated responses occur in rat thoracic aorta.

Subjects/Keywords: Rats; Vascular smooth muscle; Serotonin

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APA (6^th Edition):

Edgington, N. P. (1992). Characterization of 5-Hydroxytryptamine-Evoked Isometric Contractile Responses in Aortic Vascular Smooth Muscle in Thyropathological Rats . (Thesis). Drake U. Retrieved from http://hdl.handle.net/2092/615

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):

Edgington, Nicholas P. “Characterization of 5-Hydroxytryptamine-Evoked Isometric Contractile Responses in Aortic Vascular Smooth Muscle in Thyropathological Rats .” 1992. Thesis, Drake U. Accessed January 24, 2021. http://hdl.handle.net/2092/615.

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

MLA Handbook (7^th Edition):

Edgington, Nicholas P. “Characterization of 5-Hydroxytryptamine-Evoked Isometric Contractile Responses in Aortic Vascular Smooth Muscle in Thyropathological Rats .” 1992. Web. 24 Jan 2021.

Vancouver:

Edgington NP. Characterization of 5-Hydroxytryptamine-Evoked Isometric Contractile Responses in Aortic Vascular Smooth Muscle in Thyropathological Rats . [Internet] [Thesis]. Drake U; 1992. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/2092/615.

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

Council of Science Editors:

Edgington NP. Characterization of 5-Hydroxytryptamine-Evoked Isometric Contractile Responses in Aortic Vascular Smooth Muscle in Thyropathological Rats . [Thesis]. Drake U; 1992. Available from: http://hdl.handle.net/2092/615

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

University of Manitoba

25. 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 (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 24, 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. 24 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 24]. 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 Glasgow

26. Ighoroje, Ahbor Dolly Awani. pH and vascular tone.

Degree: PhD, 1987, University of Glasgow

URL: http://theses.gla.ac.uk/77493/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293493

► The mechanisms by which extracellular pH (pH0) and intracellular pH (pHi) affect vascular tone, and by which pHi itself is regulated in the vascular smooth… (more)

▼ The mechanisms by which extracellular pH (pH0) and intracellular pH (pHi) affect vascular tone, and by which pHi itself is regulated in the vascular smooth muscle cells, have been investigated. The majority of experiments were carried out with isolated rabbit ears activated with 10 -6M noradrenaline and perfused at constant flow. Other preparations studied were perfused whole femoral beds of rabbits and frog whole body. The perfusing solutions were phosphate, Hepes or CO2 / HCO3- buffered Ringer's having Cl- as the bulk anion, and appropiately oxygenated. pHi was modified at constant pH0 using two different procedures, one was the application and withdrawal of CO2 and the other was the "NH4+ pulse" technique, which involved the application and washout of NH4+. The procedures which can be expected to lower pHi at constant pH0 both raised tone while the reverse steps reduced it. With every fluid used NH4+ application or lowering / withdrawal of CO2 dilated the vascular bed while NH4+ withdrawal or elevation / application of CO2 constricted it. The time courses of the changes in tone were reminiscent of pH responses to the above procedures, shown by intracellular pH electrode measurement in various cell types e. g. vas deferens (Aicken, 1984), squid giant axon (Thomas, 1974, '84) and pHi estimations by N. M. R. techniques with mixed arterial preparations (Dawson, Spurway and Wray, 1985) - in all these cases extracellular NH4+ transiently raises cytoplasmic pH while the subsequent washout carries it for a period below the control level. By contrast with the mammalian preparations NH4+ application actually vasoconstricted while its withdrawal vasodilated. The phenomena were investigated under varying ionic and external conditions and were compared under three pH0's: 6.7, 7.2, 7.7. There were no qualitative differences under all conditions though quantitatively there were variations. The results excluded all the explanations of the classical pH0 effect invoking direct H+ inhibition of intracellular events. Therefore displacement of Ca2+ by H+ from sequestering sites (S. R; mitochondria) other than the myofibrils themselves was proposed to account for these pHi effects observed. Some interventions, known to affect pHi homeostasis in other cells, were employed to establish possible mechanisms of pHi regulation. Replacement of all Cl- with PhSO3-, or H2PO4- with HCO3, and the application of S.I.T.S. or amiloride all retarded the adaptation of tone from NH4+ dilatation. Replacement of all NaO+ with Li+, choline, sucrose or K+, replacement of H2 PO4 with HCO3- and applications of S.I.T.S. , ouabain, amiloride and its derivatives all retarded to varying degrees the adaptation of tone from the washout constriction. Notably among the latter was the 10x greater potency of a claimed Na+ - H+ exchange inhibitor than of a claimed 2Na+ -Ca2+ inhibitor. Quantitative considerations such as this lead to the conclusion that Cl- -HCO3- exchange plays the major role in the elimination of alkaline load while excess H+i are eliminated mainly…

Subjects/Keywords: 590; Vascular smooth muscle

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APA (6^th Edition):

Ighoroje, A. D. A. (1987). pH and vascular tone. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/77493/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293493

Chicago Manual of Style (16^th Edition):

Ighoroje, Ahbor Dolly Awani. “pH and vascular tone.” 1987. Doctoral Dissertation, University of Glasgow. Accessed January 24, 2021. http://theses.gla.ac.uk/77493/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293493.

MLA Handbook (7^th Edition):

Ighoroje, Ahbor Dolly Awani. “pH and vascular tone.” 1987. Web. 24 Jan 2021.

Vancouver:

Ighoroje ADA. pH and vascular tone. [Internet] [Doctoral dissertation]. University of Glasgow; 1987. [cited 2021 Jan 24]. Available from: http://theses.gla.ac.uk/77493/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293493.

Council of Science Editors:

Ighoroje ADA. pH and vascular tone. [Doctoral Dissertation]. University of Glasgow; 1987. Available from: http://theses.gla.ac.uk/77493/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293493

University of Manchester

27. Lewis, Sophronia. The effect of ablation and acute inhibition of plasma membrane calcium ATPase 4 (PMCA4) with a novel inhibitor on isolated mouse mesenteric resistance arterial contractility.

Degree: PhD, 2013, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/the-effect-of-ablation-and-acute-inhibition-of-plasma-membrane-calcium-atpase-4-pmca4-with-a-novel-inhibitor-on-isolated-mouse-mesenteric-resistance-arterial-contractility(676a26ea-867e-4947-9544-76b356fce23a).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.574288

► Plasma membrane calcium ATPase 4 (PMCA4) is a calcium extrusion pump which may also modulate Ca2+-triggered signal transduction pathways. Previous studies postulate that PMCA4 modulates… (more)

▼ Plasma membrane calcium ATPase 4 (PMCA4) is a calcium extrusion pump which may also modulate Ca2+-triggered signal transduction pathways. Previous studies postulate that PMCA4 modulates signalling via an interaction with neuronal nitric oxide synthase (nNOS) in localised plasmalemmal microdomains. The effect of PMCA4 on vascular contractility is unclear. This project has utilised PMCA4 ablated mice (PMCA4 KO (-/-)) and a novel specific PMCA4 inhibitor (termed AP2) to study the role of PMCA4 in mouse resistance artery contractility.Immunohistochemistry, Western blotting and polymerase chain reaction (PCR) confirmed the absence of PMCA4 in the brain, vasculature and ear snips obtained from PMCA4 KO (-/-) mice whereas it was present in those from wild type (WT (+/+)) mice. Pressure myography was employed to assesss contractile function of isolated, pressurised (to 60 mmHg) mesenteric resistance arteries from 3 months old male PMCA4 KO (-/-) and WT (+/+) mice, in response to high K+ physiological salt solution (KPSS) (40mM & 100mM) and noradrenaline (NA) (Log[NA] -9.0 to -5.0M). Passive lumen diameter and left and right wall thicknesses of arteries from PMAC4 KO (-/-) and WT (+/+) mice were taken at transmural pressures of 5-140 mmHg. Effects of acute PMCA4 inhibition with AP2 (10µM and 1µM), nitric oxide synthase (NOS) inhibition with LNNA (100µM) and specific nNOS inhibition with Vinyl-L-Nio (10µM) were also investigated. Effects of PMCA4 ablation and AP2 (10µM) on global intracellular Ca2+ changes ([Ca2+]i) in pressurised mesenteric arteries were assessed after loading arteries with the Ca2+-sensitive indicator indo-1. PMCA4 ablation had no effect on the magnitude of arterial constrictions or on the changes of [Ca2+]i in response to KPSS (40mM & 100mM) or to noradrenaline. The passive intra-lumen diameter, wall thickness, wall to lumen diameter and cross sectional area of mesenteric arteries across the intravascular pressure range studied were also not modulated by PMCA4 ablation. A leftwards shift in the stress to strain relationship and significant increase in beta elastic modulus (β) were revealed in arteries from PMCA4 KO (-/-) mice compared to those from WT (+/+) mice, suggesting that PMCA4 ablation reduces mesenteric arterial distensibility. Acute PMCA4 inhibition with AP2, significantly reduced arterial constrictions and the increase in [Ca2+]i in response to noradrenaline in arteries from WT (+/+) mice, but had no effect on arterial constrictions elicited by arteries from PMCA4 KO (-/-) mice. Inhibitory effects of AP2 were not present in arteries after NOS inhibition by LNNA and also after nNOS inhibition with Vinly-L-Nio. Hence, PMCA4 inhibition with AP2 reduces vascular constriction by a nNOS-dependent mechanism.In conclusion, the main findings of the study were that ablation and acute inhibition of PMCA4 with AP2 have different effects on mouse mesenteric resistance arterial contractility. This study provides more insight into PMCA4 as a significant modulator of signalling within the vasculature via effects…

Subjects/Keywords: 573.156; PMCA; contractility; calcium; arteries; vascular smooth muscle; nNOS

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

APA (6^th Edition):

Lewis, S. (2013). The effect of ablation and acute inhibition of plasma membrane calcium ATPase 4 (PMCA4) with a novel inhibitor on isolated mouse mesenteric resistance arterial contractility. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/the-effect-of-ablation-and-acute-inhibition-of-plasma-membrane-calcium-atpase-4-pmca4-with-a-novel-inhibitor-on-isolated-mouse-mesenteric-resistance-arterial-contractility(676a26ea-867e-4947-9544-76b356fce23a).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.574288

Chicago Manual of Style (16^th Edition):

Lewis, Sophronia. “The effect of ablation and acute inhibition of plasma membrane calcium ATPase 4 (PMCA4) with a novel inhibitor on isolated mouse mesenteric resistance arterial contractility.” 2013. Doctoral Dissertation, University of Manchester. Accessed January 24, 2021. https://www.research.manchester.ac.uk/portal/en/theses/the-effect-of-ablation-and-acute-inhibition-of-plasma-membrane-calcium-atpase-4-pmca4-with-a-novel-inhibitor-on-isolated-mouse-mesenteric-resistance-arterial-contractility(676a26ea-867e-4947-9544-76b356fce23a).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.574288.

MLA Handbook (7^th Edition):

Lewis, Sophronia. “The effect of ablation and acute inhibition of plasma membrane calcium ATPase 4 (PMCA4) with a novel inhibitor on isolated mouse mesenteric resistance arterial contractility.” 2013. Web. 24 Jan 2021.

Vancouver:

Lewis S. The effect of ablation and acute inhibition of plasma membrane calcium ATPase 4 (PMCA4) with a novel inhibitor on isolated mouse mesenteric resistance arterial contractility. [Internet] [Doctoral dissertation]. University of Manchester; 2013. [cited 2021 Jan 24]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-effect-of-ablation-and-acute-inhibition-of-plasma-membrane-calcium-atpase-4-pmca4-with-a-novel-inhibitor-on-isolated-mouse-mesenteric-resistance-arterial-contractility(676a26ea-867e-4947-9544-76b356fce23a).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.574288.

Council of Science Editors:

Lewis S. The effect of ablation and acute inhibition of plasma membrane calcium ATPase 4 (PMCA4) with a novel inhibitor on isolated mouse mesenteric resistance arterial contractility. [Doctoral Dissertation]. University of Manchester; 2013. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-effect-of-ablation-and-acute-inhibition-of-plasma-membrane-calcium-atpase-4-pmca4-with-a-novel-inhibitor-on-isolated-mouse-mesenteric-resistance-arterial-contractility(676a26ea-867e-4947-9544-76b356fce23a).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.574288

University of Cambridge

28. 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 24, 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. 24 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 24]. 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 Western Ontario

29. Leung, Sharon Z. The Role of Sirtuin 6 in Maintaining Vascular Integrity.

Degree: 2016, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/3676

► Oxidative stress is an underlying cause for vascular pathologies including inflammation, hypertension, and atherosclerosis. Sirtuins (SIRTs) are a family of NAD+ dependent deacetylases with pronounced… (more)

Subjects/Keywords: SIRT6; vascular smooth muscle cell; angiotensin II; inflammation; Biochemistry

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

APA (6^th Edition):

Leung, S. Z. (2016). The Role of Sirtuin 6 in Maintaining Vascular Integrity. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/3676

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):

Leung, Sharon Z. “The Role of Sirtuin 6 in Maintaining Vascular Integrity.” 2016. Thesis, University of Western Ontario. Accessed January 24, 2021. https://ir.lib.uwo.ca/etd/3676.

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

MLA Handbook (7^th Edition):

Leung, Sharon Z. “The Role of Sirtuin 6 in Maintaining Vascular Integrity.” 2016. Web. 24 Jan 2021.

Vancouver:

Leung SZ. The Role of Sirtuin 6 in Maintaining Vascular Integrity. [Internet] [Thesis]. University of Western Ontario; 2016. [cited 2021 Jan 24]. Available from: https://ir.lib.uwo.ca/etd/3676.

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

Council of Science Editors:

Leung SZ. The Role of Sirtuin 6 in Maintaining Vascular Integrity. [Thesis]. University of Western Ontario; 2016. Available from: https://ir.lib.uwo.ca/etd/3676

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

University of Aberdeen

30. McKean, Jenny Susan. The role of the cAMP mediator Epac in vascular smooth muscle cell migration.

Degree: PhD, 2015, University of Aberdeen

URL: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152502750005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.659069

► Surgical intervention can result in endothelial denudation, driving growth factor-stimulated vascular smooth muscle cell (VSMC) migration towards the intima, leading to luminal narrowing and restenosis.… (more)

▼ Surgical intervention can result in endothelial denudation, driving growth factor-stimulated vascular smooth muscle cell (VSMC) migration towards the intima, leading to luminal narrowing and restenosis. Clinically approved PGI₂ analogues, including beraprost, activate the cyclic adenosine monophosphate (cAMP) signaling pathway to inhibit VSMC migration in vitro. This pathway is a potential therapeutic target, however the downstream proteins involved in the inhibitory effects of cAMP on migration remain unknown. The aims of this study were to determine the signalling pathways involved in inhibiting VSMC migration through cAMP downstream mediators, protein kinase A (PKA) and the more recently characterised exchange protein activated by cAMP (Epac), and delineate the mechanisms involved. In human saphenous vein VSMCs, Epac activation using an Epac analogue inhibited VSMC migration. Therapeutic concentrations of beraprost (1 nM) also resulted in an inhibition of VSMC migration. The use of fluorescence resonance energy transfer (FRET) confirmed 1 nM beraprost activated Epac, but not PKA. Epac is a guanine nucleotide exchange factor (GEF) for Rap1 thus Rap1 siRNA was used to inhibit the Epac pathway. This blocked the inhibitory effects of beraprost on VSMC migration. Epac1 was localised to the leading edge of migrating VSMCs. Another G-protein, RhoA, was investigated since it is essential for cell migration and is involved in several processes including actin regulation. Epac signaling inhibited PDGF-induced RhoA activation and disassembled F-actin at the leading edge, where Epac1 was previously located. This indicates that beraprost activated the Epac pathway, which inhibited RhoA to decrease VSMC migration. The clinical relevance of this study has discovered the mechanisms of Epac's inhibitory action on VSMC migration and this pathway could be targeted therapeutically to reduce restenosis. In the future the potential use of beraprost on a drug eluting stent might be beneficial to prevent restenosis formation following surgical intervention.

Subjects/Keywords: 610; Coronary arteries; Vascular smooth muscle; Cell migration; Cyclic adenylic acid

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

APA (6^th Edition):

McKean, J. S. (2015). The role of the cAMP mediator Epac in vascular smooth muscle cell migration. (Doctoral Dissertation). University of Aberdeen. Retrieved from https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152502750005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.659069

Chicago Manual of Style (16^th Edition):

McKean, Jenny Susan. “The role of the cAMP mediator Epac in vascular smooth muscle cell migration.” 2015. Doctoral Dissertation, University of Aberdeen. Accessed January 24, 2021. https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152502750005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.659069.

MLA Handbook (7^th Edition):

McKean, Jenny Susan. “The role of the cAMP mediator Epac in vascular smooth muscle cell migration.” 2015. Web. 24 Jan 2021.

Vancouver:

McKean JS. The role of the cAMP mediator Epac in vascular smooth muscle cell migration. [Internet] [Doctoral dissertation]. University of Aberdeen; 2015. [cited 2021 Jan 24]. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152502750005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.659069.

Council of Science Editors:

McKean JS. The role of the cAMP mediator Epac in vascular smooth muscle cell migration. [Doctoral Dissertation]. University of Aberdeen; 2015. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152502750005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.659069

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