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You searched for subject:(eNOS activity). Showing records 1 – 2 of 2 total matches.

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University of New South Wales

1. Rodriguez, Macarena. The structure-function relationship of membrane domains in endothelial cells.

Degree: Centre for Vascular Research, 2010, University of New South Wales

Endothelial cells respond to a large range of stimuli including circulating lipoproteins, growth factors and changes in haemodynamic mechanical forces to maintain the integrity of the blood vessels and control blood pressure. These adaptive responses can be either pro- or anti-atherosclerotic. The fundamental mechanisms of these cellular responses are complex and not well understood. Many endothelial cell responses are mediated by the plasma membrane of these cells and therefore dependent on its structure and composition. The aim was to determine the role of distinct membrane lipid domains (lipid rafts) in endothelial cell responses when subjected to changes in membrane lipid composition. Experimentally, membrane lipid composition can be manipulated by enrichment with cholesterol or treatment with the oxysterol 7-ketocholesterol, which depletes cholesterol from lipid rafts. For this study bovine aortic endothelial cells (BAEC) were treated with Chol (cholesterol/mβCD complex), 7KC (7-ketocholesterol/mβCD complex) or a 1:1 mixture of the two sterols (Ch:7KC). Endothelial cell function was assessed in terms of vascular endothelial cell growth factor (VEGF), high density lipoprotein (HDL) or shear stress-induced signalling and endothelial nitric oxide (eNOS) activity. Signal transduction processes initiated by these stimuli are mediated by ordered domains at focal adhesions (FA), lipid raft domains and caveolae membrane domains respectively. Hence the structure and composition of these specific domains is important for eNOS activation and signalling. Cholesterol enrichment had a dramatic effect on HDL-induced eNOS activation, while shear stress- and VEGF-induced eNOS activity was not significantly increased, suggesting that non-caveolar lipid rafts are 7KC-sensitive, while membrane domains at FA are not. Different membrane domains in endothelial cells are differentially modulated by cholesterol enrichment, initiating signalling pathways and eNOS activation. This research contributes to the understanding of the function of distinct endothelial cell membrane lipid domains in mediating signalling responses. Advisors/Committee Members: Gaus, Katharina, Centre for Vascular Research, Faculty of Medicine, UNSW, Jessup, Wendy, Centre for Vascular Research, Faculty of Medicine, UNSW.

Subjects/Keywords: eNOS activity; Endothelial; Plasma membrane

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

APA (6th Edition):

Rodriguez, M. (2010). The structure-function relationship of membrane domains in endothelial cells. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/50231 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9109/SOURCE02?view=true

Chicago Manual of Style (16th Edition):

Rodriguez, Macarena. “The structure-function relationship of membrane domains in endothelial cells.” 2010. Doctoral Dissertation, University of New South Wales. Accessed October 24, 2020. http://handle.unsw.edu.au/1959.4/50231 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9109/SOURCE02?view=true.

MLA Handbook (7th Edition):

Rodriguez, Macarena. “The structure-function relationship of membrane domains in endothelial cells.” 2010. Web. 24 Oct 2020.

Vancouver:

Rodriguez M. The structure-function relationship of membrane domains in endothelial cells. [Internet] [Doctoral dissertation]. University of New South Wales; 2010. [cited 2020 Oct 24]. Available from: http://handle.unsw.edu.au/1959.4/50231 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9109/SOURCE02?view=true.

Council of Science Editors:

Rodriguez M. The structure-function relationship of membrane domains in endothelial cells. [Doctoral Dissertation]. University of New South Wales; 2010. Available from: http://handle.unsw.edu.au/1959.4/50231 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9109/SOURCE02?view=true


University of Maryland

2. Park, Joon Young. NFKB1 Gene Promoter Polymorphism and Unidirectional Laminar Shear Stress: Implications for NF-kB Activation, eNOS Protein Expression and Endothelial Function.

Degree: Kinesiology, 2006, University of Maryland

Exercise stimulus can be defined as endothelial wall shear stress. In the endothelial cells, the nuclear factor-kappa B (NF-κB) is an important intracellular signaling molecule by which changes in wall shear stress, sensed by mechanosensors, are transduced into the nucleus to initiate downstream eNOS gene expression. Recently, a polymorphism in the promoter region of the gene encoding a p50/p105 NF-κB subunit, NFKB1, has been identified. The NFKB1 ATTG insertion (I) / deletion (D) (NFKB1 I/D) promoter polymorphism transcriptionally regulates NFKB1 gene expression. However, the functional significance of this polymorphism has not been elucidated in endothelial cells under LSS and in endothelial function in humans. Therefore, the purpose of this study was to investigate whether the NFKB1 I/D promoter polymorphism had functional genetic properties in human umbilical vein endothelial cells (HUVECs) under physiological levels of unidirectional laminar shear stress (LSS), and further, whether the polymorphism was associated with changes in endothelial function after endurance exercise training in pre- and stage I hypertensive individuals. The major findings of the present study were that 1) a protein present in HUVECs preferentially and specifically binds to the I allele promoter compare to the D allele; 2) the I allele had significantly higher promoter activity than the D allele; and accordingly, the II homozygote cells had higher p50/p105 NFKB1 protein levels than the DD homozygote cells; 3) the II homozygote cells showed a greater increase in eNOS protein levels than the DD homozygote cells under unidirectional LSS; and 4) the I-allele carrier group had a greater reactive hyperemic forearm blood flow response, a measure of endothelial function, before exercise training; however, the NFKB1 I/D polymorphism was not significantly associated with the differential changes in endothelial function following exercise training. These results have potential clinical implications for endothelial dysfunction that are related to the development and progression of atherosclerosis and cardiovascular disease. In addition, our findings provide insight into the molecular mechanisms involved in the intracellular signaling transduction process of eNOS gene expression and function of the NFKB1 gene promoter region. Advisors/Committee Members: Brown, Michael D. (advisor).

Subjects/Keywords: Biology, Molecular; Biology, Animal Physiology; Biology, Cell; NF-kB; laminar shear stress; eNOS; promoter sequence variation; physical activity; endothelial function

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

APA (6th Edition):

Park, J. Y. (2006). NFKB1 Gene Promoter Polymorphism and Unidirectional Laminar Shear Stress: Implications for NF-kB Activation, eNOS Protein Expression and Endothelial Function. (Thesis). University of Maryland. Retrieved from http://hdl.handle.net/1903/3646

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

Chicago Manual of Style (16th Edition):

Park, Joon Young. “NFKB1 Gene Promoter Polymorphism and Unidirectional Laminar Shear Stress: Implications for NF-kB Activation, eNOS Protein Expression and Endothelial Function.” 2006. Thesis, University of Maryland. Accessed October 24, 2020. http://hdl.handle.net/1903/3646.

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

MLA Handbook (7th Edition):

Park, Joon Young. “NFKB1 Gene Promoter Polymorphism and Unidirectional Laminar Shear Stress: Implications for NF-kB Activation, eNOS Protein Expression and Endothelial Function.” 2006. Web. 24 Oct 2020.

Vancouver:

Park JY. NFKB1 Gene Promoter Polymorphism and Unidirectional Laminar Shear Stress: Implications for NF-kB Activation, eNOS Protein Expression and Endothelial Function. [Internet] [Thesis]. University of Maryland; 2006. [cited 2020 Oct 24]. Available from: http://hdl.handle.net/1903/3646.

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

Council of Science Editors:

Park JY. NFKB1 Gene Promoter Polymorphism and Unidirectional Laminar Shear Stress: Implications for NF-kB Activation, eNOS Protein Expression and Endothelial Function. [Thesis]. University of Maryland; 2006. Available from: http://hdl.handle.net/1903/3646

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

.