期刊
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
卷 44, 期 6, 页码 1031-1039出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.biocel.2012.03.013
关键词
PGF(2 alpha); Collagen; FP receptor; PKC; Rho kinase
资金
- Key Technologies R&D Program of Shandong Province [2006GG2202020, 2010G0020262]
- Natural Science Foundation of Shandong Province [Y2005C11, ZR2009CM022, ZR2009CM025, BS2009YY026]
- National Natural Science Foundation of China [30871038, 30971215, 81070192, 81070141, 81100605]
- National Basic Research Program of China (973 Program) [2012CB722406]
Accumulation of collagen I and III in the myocardium is a prominent feature of interstitial fibrosis. Prostaglandin F-2 alpha (PGF(2 alpha)) facilitates fibrosis by increasing collagen synthesis. However, the underlying mechanisms mediating the effect of PGF(2 alpha) on collagen expression in cardiac fibroblasts are not yet fully elucidated. We measured the mRNA and protein levels of collagen land III by quantitative real-time PCR and ELISA, respectively. Activation of signaling pathways was determined by western blot analysis. In primary rat cardiac fibroblasts, treatment with PGF(2 alpha) stimulated both the mRNA and protein levels of collagen land III, and pretreatment with the F-prostanoid (FP) receptor antagonist AL-8810, protein kinase C inhibitor LY-333531, and Rho kinase inhibitor Y-27632 significantly inhibited PGF(2 alpha)-induced collagen I and III expression. FP receptor, protein kinase C. and Rho kinase were activated with PGF(2 alpha) treatment. PGF(2 alpha) may be an important regulator in the synthesis of collagen I and Ill via an FP receptor/protein kinase C/Rho kinase cascade in cardiac fibroblasts, which might be a new therapeutic target for myocardial fibrosis. Published by Elsevier Ltd.
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