Knockdown of plasmacytoma variant translocation 1 (PVT1) inhibits high glucose-induced proliferation and renal fibrosis in HRMCs by regulating miR-23b-3p/early growth response factor 1 (EGR1)

Long noncoding RNAs (lncRNAs) have been reported to play critical role in the development of diabetic nephropathy (DN). However, effects and mechanism plasmacytoma variant translocation 1 (PVT1) remain poorly understood. The expression PVT1, miR-23b-3p, early growth response factor (EGR1), Fibronectin (FN), Collagen IV (Col IV), alpha smooth muscle actin (α-SMA), E-cadherin, vimentin, transforming (TGF)-β1 was examined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation assessed Counting-8 (CCK-8) assay. Western blot assay conducted measure protein levels FN, Col IV, α-SMA, TGF-β1, EGR1. interaction between miR-23b-3p PVT1 or EGR1 predicted starBase TargetScan confirmed dual luciferase reporter oxidative stress factors were analyzed corresponding kits. We found that increased decreased serum samples DN patients HG-induced HRMCs. Knockdown significantly inhibited proliferation, extracellular matrix (ECM) accumulation, epithelial-mesenchymal transition (EMT), HRMCs, while these abated inhibiting miR-23b-3p. In addition, as downstream target could specially bind PVT1. Besides, downregulation progression partially via upregulating downregulating conclusion, our results suggested knockdown suppressed though functioning ceRNA regulate vitro, providing potential value for treatment DN.