Abstract
Fibroblasts release prostaglandins and express a range of prostanoid receptors. However the importance of prostaglandins in fibroblast biology have not been fully explored. Our studies showed that the prostaglandin metabolite PGI(2) blocks the activation of fibroblasts, antagonising the induction of Ras/MEK/ERK signalling by TGFbeta. Endogenous PGI(2) acts so as to limit the activation of fibroblasts following tissue injury. By contrast PGE(2) induced in injured tissues or disease states may promote recruitment of inflammatory cells and lead to secondary activation of fibroblasts. The effects of PGI(2) on cell signaling could be manipulated to inhibit fibrosis in patients.