High Glucose-Induced Human Kidney Cell Apoptosis and Inflammatory Injury Are Alleviated by Circ_0008529 Knockdown via Circ_0008529-Mediated miR-485-5p/WNT2B Signaling.

Human kidney cell injury is a representative characteristic of diabetic nephropathy (DN), and its development has been shown to be associated with the dysregulation of some circular RNAs (circRNAs). We thus explored the role of circ_0008529 in DN-conditioned human kidney cell injury. Human kidney cells (HK-2) were treated with high glucose (HG) to construct DN models in vitro. Quantitative real-time PCR (qPCR) assay and western blot assay were used for expression detection of circ_0008529, miR-485-5p, and Wnt family member 2B (WNT2B). Cell viability was ascertained by CCK-8 assay. Cell apoptosis was assessed by flow cytometry assay and the expression levels of apoptosis-related markers. The release of inflammatory factors was examined by ELISA. The putative binding relationship between miR-485-5p and circ_0008529 or WNT2B was further verified by dual-luciferase reporter experiment, RIP assay, and pull-down assay. Circ_0008529 was highly expressed in serum of DN patients and HG-treated HK-2 cells. HG largely impaired cell viability and promoted cell apoptosis and inflammation production, while circ_0008529 knockdown attenuated the effects of HG. Circ_0008529 targeted miR-485-5p, and miR-485-5p inhibition recovered HK-2 cell injury that was blocked by circ_0008529 knockdown. In addition, miR-485-5p bound to WNT2B whose expression was positively modulated by circ_0008529. WNT2B overexpression recovered the inhibition of HK-2 cell injury caused by miR-485-5p upregulation. Circ_0008529 targeted the miR-485-5p/WNT2B pathway to regulate HG-induced HK-2 cell apoptosis and inflammatory injury, suggesting that circ_0008529 was a vital regulator in DN development.