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Fluid Shear Stress and Fibroblast Growth Factor-2 Increase Endothelial Cell-Associated Vitronectin

Vitronectin is a matricellular protein that plays an important role in both coagulation and angiogenesis through its effects on cell adhesion and the plasminogen system. Vitronectin is known to bind to endothelial cells upon integrin activation. However, the effect of integrin activation by shear st...

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Autores principales: Mathew, Justin G., Basehore, Sarah, Clyne, Alisa Morss
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5474279/
https://www.ncbi.nlm.nih.gov/pubmed/28659710
http://dx.doi.org/10.1155/2017/9040161
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author Mathew, Justin G.
Basehore, Sarah
Clyne, Alisa Morss
author_facet Mathew, Justin G.
Basehore, Sarah
Clyne, Alisa Morss
author_sort Mathew, Justin G.
collection PubMed
description Vitronectin is a matricellular protein that plays an important role in both coagulation and angiogenesis through its effects on cell adhesion and the plasminogen system. Vitronectin is known to bind to endothelial cells upon integrin activation. However, the effect of integrin activation by shear stress and growth factors on cell-associated vitronectin and plasminogen system activity has not yet been studied. We therefore exposed human umbilical vein endothelial cells to steady laminar flow, oscillating disturbed flow, or fibroblast growth factor-2 (FGF-2) for 24 hours. We then measured cell-associated vitronectin by Western blot and plasminogen system activity using a Chromozym assay. Steady laminar flow, oscillating disturbed flow, and FGF-2 all increased cell-associated vitronectin, although the vitronectin molecular weight varied among the different conditions. FGF-2 also increased cell-associated vitronectin in microvascular endothelial cells and vascular smooth muscle cells. The increase in cell-associated vitronectin increased plasminogen system activity. Confocal microscopy showed that vitronectin was primarily located in the basal and intracellular regions. α(v)β(5) integrin inhibition via genistein, an anti-α(v)β(5) antibody, or β(5) siRNA knockdown abrogated the FGF-2-induced increase in cell-associated vitronectin and increased plasminogen system activity. These data show that shear stress and growth factors increase cell-associated vitronectin through integrin activation, which may affect coagulation and angiogenesis.
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spelling pubmed-54742792017-06-28 Fluid Shear Stress and Fibroblast Growth Factor-2 Increase Endothelial Cell-Associated Vitronectin Mathew, Justin G. Basehore, Sarah Clyne, Alisa Morss Appl Bionics Biomech Research Article Vitronectin is a matricellular protein that plays an important role in both coagulation and angiogenesis through its effects on cell adhesion and the plasminogen system. Vitronectin is known to bind to endothelial cells upon integrin activation. However, the effect of integrin activation by shear stress and growth factors on cell-associated vitronectin and plasminogen system activity has not yet been studied. We therefore exposed human umbilical vein endothelial cells to steady laminar flow, oscillating disturbed flow, or fibroblast growth factor-2 (FGF-2) for 24 hours. We then measured cell-associated vitronectin by Western blot and plasminogen system activity using a Chromozym assay. Steady laminar flow, oscillating disturbed flow, and FGF-2 all increased cell-associated vitronectin, although the vitronectin molecular weight varied among the different conditions. FGF-2 also increased cell-associated vitronectin in microvascular endothelial cells and vascular smooth muscle cells. The increase in cell-associated vitronectin increased plasminogen system activity. Confocal microscopy showed that vitronectin was primarily located in the basal and intracellular regions. α(v)β(5) integrin inhibition via genistein, an anti-α(v)β(5) antibody, or β(5) siRNA knockdown abrogated the FGF-2-induced increase in cell-associated vitronectin and increased plasminogen system activity. These data show that shear stress and growth factors increase cell-associated vitronectin through integrin activation, which may affect coagulation and angiogenesis. Hindawi 2017 2017-06-01 /pmc/articles/PMC5474279/ /pubmed/28659710 http://dx.doi.org/10.1155/2017/9040161 Text en Copyright © 2017 Justin G. Mathew et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Mathew, Justin G.
Basehore, Sarah
Clyne, Alisa Morss
Fluid Shear Stress and Fibroblast Growth Factor-2 Increase Endothelial Cell-Associated Vitronectin
title Fluid Shear Stress and Fibroblast Growth Factor-2 Increase Endothelial Cell-Associated Vitronectin
title_full Fluid Shear Stress and Fibroblast Growth Factor-2 Increase Endothelial Cell-Associated Vitronectin
title_fullStr Fluid Shear Stress and Fibroblast Growth Factor-2 Increase Endothelial Cell-Associated Vitronectin
title_full_unstemmed Fluid Shear Stress and Fibroblast Growth Factor-2 Increase Endothelial Cell-Associated Vitronectin
title_short Fluid Shear Stress and Fibroblast Growth Factor-2 Increase Endothelial Cell-Associated Vitronectin
title_sort fluid shear stress and fibroblast growth factor-2 increase endothelial cell-associated vitronectin
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5474279/
https://www.ncbi.nlm.nih.gov/pubmed/28659710
http://dx.doi.org/10.1155/2017/9040161
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