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Chloride intracellular channel 1 functions in endothelial cell growth and migration

BACKGROUND: Little is known about the role of CLIC1 in endothelium. These studies investigate CLIC1 as a regulator of angiogenesis by in vitro techniques that mimic individual steps in the angiogenic process. METHODS: Using shRNA against clic1, we determined the role of CLIC1 in primary human endoth...

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Detalles Bibliográficos
Autores principales: Tung, Jennifer J, Kitajewski, Jan
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2993651/
https://www.ncbi.nlm.nih.gov/pubmed/21040583
http://dx.doi.org/10.1186/2040-2384-2-23
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author Tung, Jennifer J
Kitajewski, Jan
author_facet Tung, Jennifer J
Kitajewski, Jan
author_sort Tung, Jennifer J
collection PubMed
description BACKGROUND: Little is known about the role of CLIC1 in endothelium. These studies investigate CLIC1 as a regulator of angiogenesis by in vitro techniques that mimic individual steps in the angiogenic process. METHODS: Using shRNA against clic1, we determined the role of CLIC1 in primary human endothelial cell behavior. RESULTS: Here, we report that reduced CLIC1 expression caused a reduction in endothelial migration, cell growth, branching morphogenesis, capillary-like network formation, and capillary-like sprouting. FACS analysis showed that CLIC1 plays a role in regulating the cell surface expression of various integrins that function in angiogenesis including β1 and α3 subunits, as well as αVβ3 and αVβ5. CONCLUSIONS: Together, these results indicate that CLIC1 is required for multiple steps of in vitro angiogenesis and plays a role in regulating integrin cell surface expression.
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spelling pubmed-29936512010-11-30 Chloride intracellular channel 1 functions in endothelial cell growth and migration Tung, Jennifer J Kitajewski, Jan J Angiogenes Res Research BACKGROUND: Little is known about the role of CLIC1 in endothelium. These studies investigate CLIC1 as a regulator of angiogenesis by in vitro techniques that mimic individual steps in the angiogenic process. METHODS: Using shRNA against clic1, we determined the role of CLIC1 in primary human endothelial cell behavior. RESULTS: Here, we report that reduced CLIC1 expression caused a reduction in endothelial migration, cell growth, branching morphogenesis, capillary-like network formation, and capillary-like sprouting. FACS analysis showed that CLIC1 plays a role in regulating the cell surface expression of various integrins that function in angiogenesis including β1 and α3 subunits, as well as αVβ3 and αVβ5. CONCLUSIONS: Together, these results indicate that CLIC1 is required for multiple steps of in vitro angiogenesis and plays a role in regulating integrin cell surface expression. BioMed Central 2010-11-01 /pmc/articles/PMC2993651/ /pubmed/21040583 http://dx.doi.org/10.1186/2040-2384-2-23 Text en Copyright ©2010 Tung and Kitajewski; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Tung, Jennifer J
Kitajewski, Jan
Chloride intracellular channel 1 functions in endothelial cell growth and migration
title Chloride intracellular channel 1 functions in endothelial cell growth and migration
title_full Chloride intracellular channel 1 functions in endothelial cell growth and migration
title_fullStr Chloride intracellular channel 1 functions in endothelial cell growth and migration
title_full_unstemmed Chloride intracellular channel 1 functions in endothelial cell growth and migration
title_short Chloride intracellular channel 1 functions in endothelial cell growth and migration
title_sort chloride intracellular channel 1 functions in endothelial cell growth and migration
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2993651/
https://www.ncbi.nlm.nih.gov/pubmed/21040583
http://dx.doi.org/10.1186/2040-2384-2-23
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