Deficiency in vitamin D and its active metabolite is a characteristic of chronic kidney diseases (CKDs). Previous studies have reported that 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3], the active form of vitamin D, can attenuate renal interstitial fibrosis. The present study aimed to explore the effect of 1,25(OH)2D3 on the transdifferentiation of NRK-52E rat renal tubular epithelial cells (RTECs) induced by high glucose, as well as the expression of vitamin D receptor (VDR) and production of angiotensin (Ang) II. Western blot and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analyses were performed to detect the protein and mRNA expression of α-smooth muscle actin (α-SMA), E-cadherin and VDR. Furthermore, the production of Ang II was analyzed by enzyme-linked immunosorbent assay (ELISA). Treatment with high glucose decreased E-cadherin and VDR, while increasing α-SMA and Ang II, and of note, these changes were attenuated by 1,25(OH)2D3 in a dose-dependent manner. In conclusion, the present study revealed that 1,25(OH)2D3 inhibits high glucose-induced transdifferentiation of rat RTECs in a dose-dependent manner, which may be associated with the downregulation of Ang II and upregulation of VDR.
Keywords: 1α,25-dihydroxyvitamin D3; NRK-52E; angiotensin II; epithelial-mesenchymal transition; vitamin D receptor.