INTERLEUKIN 10 INHIBITS THE RAT VSMC PROLIFERATION AND COLLAGEN SECRETION STIMULATED BY ANGIOTENSIN II
中国医学科学杂志(英文版)2001年0卷第3期 页码:125-128
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INTERLEUKIN 10 INHIBITS THE RAT VSMC PROLIFERATION AND COLLAGEN SECRETION STIMULATED BY ANGIOTENSIN II
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This research was supported by the National Natural Sciences Foundation (No.39730220).
DOI:
中图分类号:R446.5
纸质出版日期:2001
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INTERLEUKIN 10 INHIBITS THE RAT VSMC PROLIFERATION AND COLLAGEN SECRETION STIMULATED BY ANGIOTENSIN II[J]. 中国医学科学杂志(英文版), 2001,0(3):125-128.
INTERLEUKIN 10 INHIBITS THE RAT VSMC PROLIFERATION AND COLLAGEN SECRETION STIMULATED BY ANGIOTENSIN II[J]. Chinese medical sciences journal, 2001, 0(3): 125-128.
INTERLEUKIN 10 INHIBITS THE RAT VSMC PROLIFERATION AND COLLAGEN SECRETION STIMULATED BY ANGIOTENSIN II[J]. 中国医学科学杂志(英文版), 2001,0(3):125-128.DOI:
INTERLEUKIN 10 INHIBITS THE RAT VSMC PROLIFERATION AND COLLAGEN SECRETION STIMULATED BY ANGIOTENSIN II[J]. Chinese medical sciences journal, 2001, 0(3): 125-128.DOI:
INTERLEUKIN 10 INHIBITS THE RAT VSMC PROLIFERATION AND COLLAGEN SECRETION STIMULATED BY ANGIOTENSIN II
摘要
Abstract
Objective. To study the effect of interleukin 10 (IL- 10) on the angiotensin II (AngII) stimulated rat VSMC proliferation and collagen secretion
and furthermore
explore its mechanism. Methods. On cultured VSMC of rat
3H- thymine (3H- TdR) and 3H- proline incorporations were used to evaluate the DNA and collagen synthesis
respectively. Western blot and immunoprecipitation were applied to assay the expression and activity of focal adhesion kinase (FAK)
respectively. Results. IL- 10 (10- 8~ 10- 10g/ml) inhibited the increase of 3H- TdR and 3H- proline incorporation as well as FAK activity
which was induced by 10- 7mol/L AngII (P< 0.05 or P< 0.01). IL- 10 also obviously downregulated the synthesis and secretion of collagen by AngII stimulated VSMC. But there was no difference in the protein expression of FAK among all the groups (P >0.05). Conclusion. IL- 10 antagonizes the VSMC proliferation and collagen synthesis by regulating FAK activity stimulated by AngII.