Centre for Rheumatology and Connective Tissue Diseases, Royal Free Hospital Campus, University College London, London, UK.
J Cell Commun Signal. 2010 Jun;4(2):75-7. doi: 10.1007/s12079-010-0089-8. Epub 2010 Mar 26.
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.
成纤维细胞释放前列腺素,并表达一系列前列腺素受体。然而,前列腺素在成纤维细胞生物学中的重要性尚未得到充分探索。我们的研究表明,前列腺素代谢物 PGI(2)阻断成纤维细胞的激活,拮抗 TGFβ诱导的 Ras/MEK/ERK 信号转导。内源性 PGI(2)的作用是限制组织损伤后成纤维细胞的激活。相比之下,在受伤组织或疾病状态下诱导的 PGE(2)可能会招募炎症细胞并导致成纤维细胞的二次激活。PGI(2)对细胞信号转导的影响可以被操纵,以抑制患者的纤维化。