TMEM72/SCPx TRIGGERED-LIPID ACCUMULATION IN RENAL TUBULAR EPITHELIAL CELLS CONTRIBUTES TO DIABETIC KIDNEY DISEASE

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TMEM72/SCPx TRIGGERED-LIPID ACCUMULATION IN RENAL TUBULAR EPITHELIAL CELLS CONTRIBUTES TO DIABETIC KIDNEY DISEASE

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Co-author 1

Jianteng Xie 13826495245@139.com South China University of Technology School of Medicine Guangzhou China * The Affiliated Panyu Central Hospital of Guangzhou Medical University Nephrology Department Guangzhou China

Co-author 2

Runli Jia 1633309377@qq.com Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences Nephrology Department Guangzhou China - South China University of Technology School of Medicine Guangzhou China

Co-author 3

Danfeng Liu 202220156990@scut.edu.cn South China University of Technology School of Medicine Guangzhou China -

Co-author 4

Xuan Zhao 1328238937@qq.com Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences Nephrology Department Guangzhou China - Southern Medical University The Second School of Clinical Medicine Guangzhou China

Co-author 5

Wenjian Wang wangwenjian@gdph.org.cn Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences Nephrology Department Guangzhou China - South China University of Technology School of Medicine Guangzhou China Southern Medical University The Second School of Clinical Medicine Guangzhou China

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Introduction

Lipid accumulation in tubular epithelial cell (TEC) is an important mechanism for the progression of diabetic kidney disease (DKD) and independent of lipid level. Our previous clinical data demonstrated that transmembrane protein 72 (TMEM72) highly expressed in tubules of the kidney and associated with the decline of renal function in biopsy-proved DKD patients. This study is designed to explore the potential specific mechanism of TMEM72 involved in the development of DKD.

Methods

TECs-specific Tmem72 knockout (Tmem72-/-) mice by a Cre-LoxP recombination system and their littermate control were created to make DKD model by intraperitoneal injection of streptozocin and high-fat-diet. Single-cell sequencing and bioinformatics analysis was used to screen the involved potential signaling pathways and simulated molecular docking was used to predict key molecular Interaction model.

Results

TECs-specific knockout of Tmem72 significantly alleviates kidney injury functionally and pathologically. A marked decrease of lipids accumulation in the kidney was found in Tmem72-/- mice compared to wild type mice. Single-cell sequencing found that lipid-metabolic pathways including lipid oxidation, fatty acid degradation, and fatty acid β-oxidation in TECs were significantly inhibited in diabetic mice. In contrast, TECs-specific knockout of Tmem72 markedly enhanced fatty acid β-oxidation in TECs of DKD mice. The sterol carrier protein-x (SCPx), the main rate-limiting enzyme for fatty acid β-oxidation and encoded by the Scp2 gene was observed and verified interacting with TMEM72. Simulated molecular docking revealed TMEM72 at amino acid sites of Asn89, Asn91, Asn92, Thr261, Glu268, and Glu290 bind to SCPx at amino acid sites Arg35, Thr30, Ser53, Pro267, and Gln63 through hydrogen bonding. In vitro, knock-down of Tmem72 or SCPx respectively or simultaneously consequently resulted in the inhibition of SCPx-mediated fatty acid β-oxidation and protected the high-glucose treated HK-2 cells evidenced by significantly increase of lipid-decomposition and reduction of lipid-accumulation.

Conclusion

Current study prided strong evidence that HG stimulated TMEM72 promoted the lipid accumulation in TECs by combined with SCPx, suggesting that TMEM72/SCPx can be a promise therapeutic target for DKD.

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