REG1A-mediated the progression of early diabetic nephropathy through regulating autophagy and fibrosis

Autophagy deficiency is a clinical feature of early diabetic nephropathy (EDN). This study aimed to investigate the role of REG1A in EDN. Rat renal proximal tubular epithelial cells were exposed to high glucose (HG) to establish in vitro EDN model. mRNA expression was determined using RT-qPCR. Protein expression was determined using Western blot. LC3 expression was determined using immunofluorescence. The location of REG1A was determined using RNA FISH assay. Cytokine release was determined using ELISA assay. We found that HG promoted the inflammation and fibrosis of rat renal proximal tubular epithelial cells, whereas it inhibited autophagy. REG1A was upregulated after exposed to HG. REG1A localized in cytoplasm of rat renal proximal tubular epithelial cells. REG1A knockdown inhibited the proliferation and fibrosis of rat renal proximal tubular epithelial cells. Moreover, REG1A knockdown reversed the effects of HG exposure and promoted autophagy in rat renal proximal tubular epithelial cells. Inhibition of REG1A protects against EDN. Therefore, targeting REG1A may be a promising strategy for EDN.