Increased vascular permeability and severe renal tubular damage after ischemia-reperfusion injury in mice lacking adiponectin or T-cadherin
Yuri Tsugawa-Shimizu, Yuya Fujishima, Shunbun Kita, Satoshi Minami, Taka‐aki Sakaue, Yuto Nakamura, Tomonori Okita, Yusuke Kawachi, Shiro Fukada, Tomoko Namba‐Hamano, Yoshitsugu Takabatake, Yoshitaka Isaka, Hitoshi Nishizawa, Barbara Ranscht, Norikazu Maeda, Iichiro Shimomura
Abstract
In the kidney, T-cadherin-associated adiponectin protein existed on peritubular capillary pericytes. In an acute renal ischemia-reperfusion model, deficiency of adiponectin or T-cadherin exhibited the more progressive phenotype of renal tubular damage and increased vascular permeability, accompanied by severe pericyte loss. In vitro, adiponectin promoted exosome secretion from mouse primary pericytes in a T-cadherin-dependent manner. Adiponectin plays an important role in maintaining the capillary network and amelioration of renal tubular injury by binding to T-cadherin.