Relaxin abrogates renal interstitial fibrosis by regulating macrophage polarization via inhibition of Toll-like receptor 4 signaling

作者：Lei Chen, Minglei Sha, Li Deng, Yiping Zhu, Xingjie Wang, Chenyi Jiang, Shujie Xia, Yi Shao · 发表于：Oncotarget · 年份：2017 · DOI：10.18632/oncotarget.15483 · 被引用次数：47 · 研究领域：Pregnancy-related medical research、Pelvic floor disorders treatments、Pelvic and Acetabular Injuries

// Lei Chen 1, * , Ming-Lei Sha 2, * , Deng Li 1, * , Yi-Ping Zhu 1 , Xing-Jie Wang 1 , Chen-Yi Jiang 1 , Shu-Jie Xia 1 , Yi Shao 1 1 Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China 2 Department of Geriatric, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China * These authors are contributed equally to this work Correspondence to: Yi Shao, email: drshaoyi@163.com Keywords: renal fibrosis, relaxin, Toll-like receptor 4, macrophage polarization Received: November 08, 2016      Accepted: February 07, 2017      Published: February 18, 2017 ABSTRACT Renal fibrosis is a common feature of chronic kidney disease (CKD). To inhibit the CKD process, it is important to prevent renal fibrosis, though CKD remains incurable. Renal fibrosis can be inhibited by relaxin in several experimental models, but the mechanism of relaxin for antifibrotic potential is still not clear. And here we have studied the role of relaxin in macrophage polarization and renal inflammation after unilateral ureteral obstruction (UUO). Our results show that relaxin can downregulate the Toll-like receptor (TLR) 4 signaling, shift macrophage polarization toward the M2 phenotype and ameliorat renal fibrosis in the early stages of UUO. In vitro experiments, it has been confirmed that relaxin can downregulate the TLR4 signaling and induce the M2 macrophage transiti...