Role of caveolin-1 on membrane estrogen receptor mediated proliferation of endothelial progenitor cells / 中华心血管病杂志
Chinese Journal of Cardiology
; (12): 1044-1047, 2011.
Article
in Chinese
| WPRIM (Western Pacific)
| ID: wpr-268260
Responsible library:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the potential role of caveolin-1 (CAV-1) on membrane estrogen receptor (mER) mediated proliferation of endothelial progenitor cells (EPCs).</p><p><b>METHODS</b>Bone marrow (BM)-derived EPCs were cultured. The proliferation of EPCs induced by estradiol (E₂)-BSA in the absence or presence of ICI 182, 780 (a pure ER inhibitor), MβCD and CAV-1 siRNA was determined by [³H]-thymidine incorporation. The expression of CAV-1 was detected by Western blot.</p><p><b>RESULTS</b>Proliferation of EPC peaked after 10(-8) mol/L E₂-BSA culture for 24 h (87.5% increase vs. control), and this effect could be inhibited by estrogen receptor blocker ICI 182, 780, indicating that mER-initiated membrane signaling pathways was involved in the proliferation effect of estrogen on EPC. Both cholesterol depletion and CAV-1 siRNA significantly attenuated E₂-BSA induced [³H]-thymidine incorporation. Western blot result confirmed that cholesterol depletion or CAV-1 siRNA significantly decreased CAV-1 protein expression (-18.6% or -41.2% vs. 10(-8) mol/L E₂-BSA alone).</p><p><b>CONCLUSION</b>Our results suggested that estradiol promoted EPC proliferation through activating CAV-1 pathway.</p>
Full text:
Available
Database:
WPRIM (Western Pacific)
Main subject:
Pharmacology
/
Stem Cells
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Endothelium, Vascular
/
Receptors, Estrogen
/
Cells, Cultured
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Rats, Sprague-Dawley
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Cell Biology
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Endothelial Cells
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Cell Proliferation
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Allergy and Immunology
Limits:
Animals
Language:
Chinese
Journal:
Chinese Journal of Cardiology
Year:
2011
Document type:
Article