Podocyte apoptosis in diabetic nephropathy by BASP1 activation of the p53 pathway via WT1

• DOI: 10.1111/apha.13634
• Publication Date: 2021-02-22T08:11:15Z
• Authors: Yingying Zhang; Chengxian Xu; Qing Ye; Lingxiao Tong; Hong Jiang; Xiujuan Zhu; Limin Huang; Weiqiang Lin; Haidong Fu; Jingjing Wang; Pontus B. Persson; En Yin Lai; Jianhua Mao
• Keywords: Slit diaphragm; Knockout mouse

Abstract Aims Diabetic nephropathy (DN) is a leading cause of end‐stage renal disease. BASP1 (brain acid‐soluble protein) up‐regulated in podocyte‐specific protein phosphatase 2A knockout mice (Pod‐PP2A‐KO) that develop kidney dysfunction. Here, we explore the role for podocytes DN. Methods was assessed kidneys from DN patients and mouse models, podocyte specific (Pod‐BASP1‐KO mice) were generated studied vivo. Furthermore, injury apoptosis measured after knockdown overexpression cell line (MPC5). Potential signalling pathways involved detected. Results expression compared to normal controls. deletion protected against by reducing loss slit diaphragm molecules foot process effacement model. promoted actin cytoskeleton rearrangements MPC5 line. Molecules p53 pathway down‐regulated treated with high glucose P53 activation through co‐repression Wilms' tumour 1 transcription factor (WT1). Conclusion activates modulation WT1 induce diabetic nephropathy.