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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...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2017
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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. |
format | Online Article Text |
id | pubmed-5474279 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
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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