Modulation of Vascular Cell Function by Bim Expression

Apoptosis of vascular cells, including pericytes and endothelial cells, contributes to disease pathogenesis in which vascular rarefaction plays a central role. Bim is a proapoptotic protein that modulates not only apoptosis but also cellular functions such as migration and extracellular matrix (ECM...

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Main Authors: Margaret E. Morrison, Tammy L. Palenski, Nasim Jamali, Nader Sheibani, Christine M. Sorenson
Format: Article
Language:English
Published: Wiley 2013-01-01
Series:International Journal of Cell Biology
Online Access:http://dx.doi.org/10.1155/2013/297537
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author Margaret E. Morrison
Tammy L. Palenski
Nasim Jamali
Nader Sheibani
Christine M. Sorenson
author_facet Margaret E. Morrison
Tammy L. Palenski
Nasim Jamali
Nader Sheibani
Christine M. Sorenson
author_sort Margaret E. Morrison
collection DOAJ
description Apoptosis of vascular cells, including pericytes and endothelial cells, contributes to disease pathogenesis in which vascular rarefaction plays a central role. Bim is a proapoptotic protein that modulates not only apoptosis but also cellular functions such as migration and extracellular matrix (ECM) protein expression. Endothelial cells and pericytes each make a unique contribution to vascular formation and function although the details require further delineation. Here we set out to determine the cell autonomous impact of Bim expression on retinal endothelial cell and pericyte function using cells prepared from Bim deficient (Bim−/−) mice. Bim−/− endothelial cells displayed an increased production of ECM proteins, proliferation, migration, adhesion, and VEGF expression but, a decreased eNOS expression and nitric oxide production. In contrast, pericyte proliferation decreased in the absence of Bim while migration, adhesion, and VEGF expression were increased. In addition, we demonstrated that the coculturing of either wild-type or Bim−/− endothelial cells with Bim−/− pericytes diminished their capillary morphogenesis. Thus, our data further emphasizes the importance of vascular cell autonomous regulatory mechanisms in modulation of vascular function.
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spelling doaj-art-282295a22ebc4e66a46745147bc671262025-08-20T03:54:38ZengWileyInternational Journal of Cell Biology1687-88761687-88842013-01-01201310.1155/2013/297537297537Modulation of Vascular Cell Function by Bim ExpressionMargaret E. Morrison0Tammy L. Palenski1Nasim Jamali2Nader Sheibani3Christine M. Sorenson4Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, 600 Highland Avenue, H4/444 CSC, Madison, WI 53792-4108, USADepartment of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792, USADepartment of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792, USADepartment of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792, USADepartment of Pediatrics, University of Wisconsin School of Medicine and Public Health, 600 Highland Avenue, H4/444 CSC, Madison, WI 53792-4108, USAApoptosis of vascular cells, including pericytes and endothelial cells, contributes to disease pathogenesis in which vascular rarefaction plays a central role. Bim is a proapoptotic protein that modulates not only apoptosis but also cellular functions such as migration and extracellular matrix (ECM) protein expression. Endothelial cells and pericytes each make a unique contribution to vascular formation and function although the details require further delineation. Here we set out to determine the cell autonomous impact of Bim expression on retinal endothelial cell and pericyte function using cells prepared from Bim deficient (Bim−/−) mice. Bim−/− endothelial cells displayed an increased production of ECM proteins, proliferation, migration, adhesion, and VEGF expression but, a decreased eNOS expression and nitric oxide production. In contrast, pericyte proliferation decreased in the absence of Bim while migration, adhesion, and VEGF expression were increased. In addition, we demonstrated that the coculturing of either wild-type or Bim−/− endothelial cells with Bim−/− pericytes diminished their capillary morphogenesis. Thus, our data further emphasizes the importance of vascular cell autonomous regulatory mechanisms in modulation of vascular function.http://dx.doi.org/10.1155/2013/297537
spellingShingle Margaret E. Morrison
Tammy L. Palenski
Nasim Jamali
Nader Sheibani
Christine M. Sorenson
Modulation of Vascular Cell Function by Bim Expression
International Journal of Cell Biology
title Modulation of Vascular Cell Function by Bim Expression
title_full Modulation of Vascular Cell Function by Bim Expression
title_fullStr Modulation of Vascular Cell Function by Bim Expression
title_full_unstemmed Modulation of Vascular Cell Function by Bim Expression
title_short Modulation of Vascular Cell Function by Bim Expression
title_sort modulation of vascular cell function by bim expression
url http://dx.doi.org/10.1155/2013/297537
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AT tammylpalenski modulationofvascularcellfunctionbybimexpression
AT nasimjamali modulationofvascularcellfunctionbybimexpression
AT nadersheibani modulationofvascularcellfunctionbybimexpression
AT christinemsorenson modulationofvascularcellfunctionbybimexpression