Occurrence and development of diabetic nephropathy caused by CD63 by inhibiting Wnt-β-catenin signaling pathway

R.-D. Zhang, M. Shi

Department of Endocrinology, The Affiliated Huai’an No. 1 People’s Hospital of Nanjing Medical University, Huai’an, P.R. China. smjcl@163.com

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• Metabolism

OBJECTIVE: This study aimed to investigate the occurrence and development of diabetic nephropathy caused by CD63 by inhibiting Wnt-β-catenin signaling pathway.

PATIENTS AND METHODS: Renal tissues and normal renal tissues distant from renal lesions of patients with diabetic nephropathy treated in The Affiliated Huai’an No. 1 People’s Hospital of Nanjing Medical University from January 2018 to November 2018 were selected. Human renal tubular epithelial cell HKC was purchased. CD63-siRNA group, NC group, blank group, CD63-mimics, CD63-mimics+si-Wnt4, and CD63-inhibitor+sh-Wnt4 were transfected into renal tubular epithelial cell HKC; mRNA expression in the cells was detected by qRT-PCR, and the protein expression in the cells was detected by WB. CCK8 and flow cytometry were used to detect cell proliferation and apoptosis.

RESULTS: CD63, Wnt4, β-catenin, and p-GSK-3β were highly expressed in diabetic nephropathy. Cell experiments showed that inhibiting CD63 and Wnt-β-catenin signaling pathway could promote cell proliferation and reduce cell apoptosis, and the protein expressions of Wnt4, β-catenin, p-GSK-3β, and Bcl-2 were significantly reduced. Rescue experiments showed that after the co-transfection of CD63-mimics+si-Wnt4 and CD63-inhibitor+sh-Wnt4 into EC109 and EC9706, the cell proliferation and apoptosis rates were not different from those of the NC group without transfection sequence.

CONCLUSIONS: CD36 can mediate cell apoptosis by inhibiting the expression of the related proteins in nodal Wnt/β-catenin signaling pathway, and is expected to become a potential therapeutic target for clinical treatment of patients with diabetic nephropathy.

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