Down-regulation of microRNA-21 reduces inflammation and podocyte apoptosis in diabetic nephropathy by relieving the repression of TIMP3 expression

Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie
Xiaoping ChenBo Lin

Abstract

Several miRNAs including miR-21 have emerged as important regulators in the development of diabetic nephropathy (DN). However, the molecular mechanism of miR-21 underlying DN pathogenesis remains to be further discussed. Streptozotocin (STZ)-induced DN rats and high glucose (HG)-induced podocytes were used as the in vivo and in vitro models of DN. miR-21 level was detected by qRT-PCR assay. Inflammatory cytokine levels were assessed by ELISA. Kidney injury of rats was evaluated by blood glucose, serum creatinine and blood urine nitrogen concentrations and periodic acid schiff (PAS) staining. Apoptosis in kidney tissues and podocytes was determined by TUNEL and flow cytometry analyses, respectively. Western blot analysis was applied to measure the protein levels of tissue inhibitors of metalloproteinase 3 (TIMP3), Bax and Bcl-2. The relationship between TIMP3 and miR-21 was confirmed by luciferase reporter assay. miR-21 expression was upregulated in serum and kidney tissues of DN patients, kidney tissues of STZ-induced DN rats, and HG-treated podocytes. miR-21 depletion inhibited pro-inflammatory factor (IL-1β, TNF-α) secretions and alleviated kidney damages in STZ-induced DN rats. Moreover, TIMP3 was a target of miR-21 in HG-tr...Continue Reading

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