Syndecan-1 shedding destroys epithelial adherens junctions through STAT3 after renal ischemia/reperfusion injury
Man Guo,
Daoqi Shen,
Yiqi Su,
Jiarui Xu,
Shuan Zhao,
Weidong Zhang,
Yaqiong Wang,
Wuhua Jiang,
Jialin Wang,
Xuemei Geng,
Xiaoqiang Ding,
Xialian Xu
Affiliations
Man Guo
Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Medical Center of Kidney Disease, Shanghai, China; Shanghai Institute of Kidney and Dialysis, Shanghai, China; Key Laboratory of Kidney and Blood Purification, Shanghai, China; Hemodialysis quality control center of Shanghai, Shanghai, China
Daoqi Shen
Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Medical Center of Kidney Disease, Shanghai, China; Shanghai Institute of Kidney and Dialysis, Shanghai, China; Key Laboratory of Kidney and Blood Purification, Shanghai, China; Hemodialysis quality control center of Shanghai, Shanghai, China
Yiqi Su
Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Medical Center of Kidney Disease, Shanghai, China; Shanghai Institute of Kidney and Dialysis, Shanghai, China; Key Laboratory of Kidney and Blood Purification, Shanghai, China; Hemodialysis quality control center of Shanghai, Shanghai, China
Jiarui Xu
Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Medical Center of Kidney Disease, Shanghai, China; Shanghai Institute of Kidney and Dialysis, Shanghai, China; Key Laboratory of Kidney and Blood Purification, Shanghai, China; Hemodialysis quality control center of Shanghai, Shanghai, China
Shuan Zhao
Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Medical Center of Kidney Disease, Shanghai, China; Shanghai Institute of Kidney and Dialysis, Shanghai, China; Key Laboratory of Kidney and Blood Purification, Shanghai, China; Hemodialysis quality control center of Shanghai, Shanghai, China
Weidong Zhang
Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Medical Center of Kidney Disease, Shanghai, China; Shanghai Institute of Kidney and Dialysis, Shanghai, China; Key Laboratory of Kidney and Blood Purification, Shanghai, China; Hemodialysis quality control center of Shanghai, Shanghai, China
Yaqiong Wang
Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Medical Center of Kidney Disease, Shanghai, China; Shanghai Institute of Kidney and Dialysis, Shanghai, China; Key Laboratory of Kidney and Blood Purification, Shanghai, China; Hemodialysis quality control center of Shanghai, Shanghai, China
Wuhua Jiang
Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Medical Center of Kidney Disease, Shanghai, China; Shanghai Institute of Kidney and Dialysis, Shanghai, China; Key Laboratory of Kidney and Blood Purification, Shanghai, China; Hemodialysis quality control center of Shanghai, Shanghai, China
Jialin Wang
Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Medical Center of Kidney Disease, Shanghai, China; Shanghai Institute of Kidney and Dialysis, Shanghai, China; Key Laboratory of Kidney and Blood Purification, Shanghai, China; Hemodialysis quality control center of Shanghai, Shanghai, China
Xuemei Geng
Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Medical Center of Kidney Disease, Shanghai, China; Shanghai Institute of Kidney and Dialysis, Shanghai, China; Key Laboratory of Kidney and Blood Purification, Shanghai, China; Hemodialysis quality control center of Shanghai, Shanghai, China
Xiaoqiang Ding
Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Medical Center of Kidney Disease, Shanghai, China; Shanghai Institute of Kidney and Dialysis, Shanghai, China; Key Laboratory of Kidney and Blood Purification, Shanghai, China; Hemodialysis quality control center of Shanghai, Shanghai, China; Corresponding author
Xialian Xu
Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Medical Center of Kidney Disease, Shanghai, China; Shanghai Institute of Kidney and Dialysis, Shanghai, China; Key Laboratory of Kidney and Blood Purification, Shanghai, China; Hemodialysis quality control center of Shanghai, Shanghai, China; Corresponding author
Summary: Adherens junctions between tubular epithelial cells are disrupted in renal ischemia/reperfusion (I/R) injury. Syndecan-1 (SDC-1) is involved in maintaining cell morphology. We aimed to study the role of SDC-1 shedding induced by renal I/R in the destruction of intracellular adherens junctions. We found that SDC-1 shedding was increased while the expression of E-cadherin was decreased. This observation was accompanied by the activation of STAT3 in the kidneys. Inhibiting the shedding of SDC-1 induced by I/R could alleviate this effect. Mild renal I/R could induce more severe renal injury, lower E-cadherin expression, damaged cell junctions, and activated STAT3 in knockout mice with the tubule-specific deletion of SDC-1 mice. The results in vitro were consistent with those in vivo. Inhibiting the shedding of SDC-1 could alleviate the decreased expression of E-cadherin and damage of cell adherens junctions through inhibiting the activation of STAT3 during ischemic acute kidney injury.
