Loss of Exoc5 in the proximal tubule exacerbates renal fibrosis following unilateral ureteral obstruction

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Loss of Exoc5 in the proximal tubule exacerbates renal fibrosis following unilateral ureteral obstruction

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Co-author 1

Hui Jae Lim ok980304@gmail.com Department of Biomedical Science and BK21 Plus, The Graduate School of Medicine Kyungpook National University Daegu Korea (Republic of) *

Co-author 2

Yong Kwon Han yonkwon3583@gmail.com Cardiovascular Research Institute Kyungpook National University Daegu Korea (Republic of) -

Co-author 3

You Ri Park youri0212@naver.com Department of Biomedical Science and BK21 Plus, The Graduate School of Medicine Kyungpook National University Daegu Korea (Republic of) -

Co-author 4

Se Young Jang magnolia1103@naver.com Department of Internal Medicine, School of Medicine Kyungpook National University Daegu Korea (Republic of) -

Co-author 5

Kwon Moo Park kmpark@knu.ac.kr Department of Anatomy, School of Medicine Kyungpook National University Daegu Korea (Republic of) -

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Introduction

Exocyst complex component 5 (Exoc5), a central component of exocyst complex, is involved in cell differentiation, which is critical for the repair process after injury. Here, we investigated the role and underlying molecular mechanisms of Exoc5 on renal fibrosis, which is a major feature of abnormal repair process and chronic kidney disease.

Methods

Kidney proximal tubule cell-specific Exoc5 knockout (PT–Exoc5KO) mice were generated by crossing Exoc5f/f mice with PEPCK-Cre mice. Wild-type (PT–Exoc5WT) and PT–Exoc5KO mice were subjected to unilateral ureteral obstruction (UUO) for 7 days and the fibrosis of the obstructive kidney was evaluated. In HK-2 cells, cultured human proximal tubule cells, EXOC5 was down-regulated using siRNA, and the fibrosis was evaluated after TGF-β treatment.

Results

PT–Exoc5KO mice showed normal renal function and structure. UUO led to renal fibrosis with decreased Exoc5 expression and Exoc5 knockout worsened the fibrosis. Exoc5 knockout alone increased Yes-associated protein (YAP) expression in the kidney and exacerbated UUO-induced YAP activation compared to PT–Exoc5WT mice. UUO induced epithelial to mesenchymal transition (EMT) and paired box 2 (Pax2) expression in both groups of mice, with greater induction in PT–Exoc5KO compared to PT–Exoc5WT mice. In HK-2 cell, a human proximal tubule cell line, knockdown of EXOC5 increased YAP expression. knockdown of EXOC5 augmented YAP activation and EMT following TGF-β treatment compared with control cells.

Conclusion

These findings indicate that Exoc5 inhibits renal fibrosis by inhibition of YAP and Pax2 expression, suggesting that research on Exoc5 may provide a novel therapeutic strategy for renal fibrosis.

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