Prostaglandin F_2¦Á facilitates collagen synthesis in cardiac fibroblasts via an F-prostanoid receptor/protein kinase C/Rho kinase pathway independent of transforming growth factor ¦Â1

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• 作者：Wen-yuan Ding¹ ; Yun Ti¹ ; Jia Wang ; Zhi-hao Wang ; Guo-lu Xie ; Yuan-yuan Shang ; Meng-xiong Tang ; Yun Zhang ; Wei Zhang ; ^{zhangweisdu@gmail.com} ; Ming Zhong ; ^{zhongmingzm@gmail.com}
• 关键词：PGF2¦Á ; Collagen ; FP receptor ; PKC ; Rho kinase
• 刊名：The International Journal of Biochemistry and Cell Biology
• 出版年：2012
• 出版时间：June, 2012
• 年：2012
• 卷：44
• 期：6
• 页码：1031-1039
• 全文大小：1235 K

文摘

Accumulation of collagen I and III in the myocardium is a prominent feature of interstitial fibrosis. Prostaglandin F_2¦Á (PGF_2¦Á) facilitates fibrosis by increasing collagen synthesis. However, the underlying mechanisms mediating the effect of PGF_2¦Á on collagen expression in cardiac fibroblasts are not yet fully elucidated. We measured the mRNA and protein levels of collagen I and 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¦Á stimulated both the mRNA and protein levels of collagen I and 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¦Á-induced collagen I and III expression. FP receptor, protein kinase C, and Rho kinase were activated with PGF_2¦Á treatment. PGF_2¦Á may be an important regulator in the synthesis of collagen I and III via an FP receptor/protein kinase C/Rho kinase cascade in cardiac fibroblasts, which might be a new therapeutic target for myocardial fibrosis.