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

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.