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: | , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | International Journal of Cell Biology |
| Online Access: | http://dx.doi.org/10.1155/2013/297537 |
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| _version_ | 1849307761560518656 |
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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. |
| format | Article |
| id | doaj-art-282295a22ebc4e66a46745147bc67126 |
| institution | Kabale University |
| issn | 1687-8876 1687-8884 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Cell Biology |
| 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 |
| work_keys_str_mv | AT margaretemorrison modulationofvascularcellfunctionbybimexpression AT tammylpalenski modulationofvascularcellfunctionbybimexpression AT nasimjamali modulationofvascularcellfunctionbybimexpression AT nadersheibani modulationofvascularcellfunctionbybimexpression AT christinemsorenson modulationofvascularcellfunctionbybimexpression |