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CD105 prevents apoptosis in hypoxic endothelial cells
Chenggang Li1, Razao Issa, Pat Kumar
1Department of Pathology, Medical School, University of Manchester and Christie Hospital, Manchester M13 9PT, UK.
Journal of Cell Science
|May 15, 2003
Summary
Hypoxia upregulates CD105 expression in endothelial cells, a key factor in blood vessel formation. This CD105 increase protects cells from apoptosis, promoting angiogenesis.
Area of Science:
- Cell Biology
- Vascular Biology
- Molecular Biology
Background:
- CD105 is an endothelial cell marker crucial for vascular development.
- Its precise regulatory mechanisms, especially under hypoxia, remain unclear.
- Hypoxia is vital for neovascularization.
Purpose of the Study:
- Investigate the role of CD105 in hypoxia-induced angiogenesis.
- Examine the effects of hypoxic stress on CD105 gene expression in endothelial cells.
Main Methods:
- Used tissue-cultured human microvascular endothelial cells.
- Analyzed CD105 gene expression, protein levels, and promoter activity under hypoxia.
- Employed antisense approach and TUNEL assay to assess CD105 function.
- Investigated apoptosis pathways (Bcl-2, Bax, Bcl-XL, Mcl-1, caspases).
Main Results:
- Hypoxia significantly increased CD105 mRNA, protein, and promoter activity.
- Hypoxia induced cell cycle arrest and apoptosis via altered Bcl-2/Bax ratio and caspase activation.
- CD105 suppression enhanced apoptosis under hypoxia.
- Hypoxia and TGF-beta1 synergistically induced apoptosis in CD105-deficient cells.
Conclusions:
- Hypoxia potently stimulates CD105 gene expression in vascular endothelial cells.
- Upregulated CD105 attenuates endothelial cell apoptosis, contributing to angiogenesis.
- CD105 plays a protective role against hypoxia-induced cell death, facilitating neovascularization.