摘要
Accumulation of collagen I and III in the myocardium is a prominent feature of interstitial fibrosis. Prostaglandin F2伪 (PGF2伪) facilitates fibrosis by increasing collagen synthesis. However, the underlying mechanisms mediating the effect of PGF2伪 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 PGF2伪 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 PGF2伪-induced collagen I and III expression. FP receptor, protein kinase C, and Rho kinase were activated with PGF2伪 treatment. PGF2伪 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.