Abstract
The abnormal expression of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) has been demonstrated to exert pivotal effects in human diseases. We focused on the functions of metastasis associated lung adenocarcinoma transcript 1 (MALAT1) and microRNA let-7f on diabetic nephropathy (DN). The diabetes (db/db) mice were treated with silenced MALAT1, then the baseline indicators, pathology changes, marker proteins of podocyte injury (nephrin, podocin, desmin and Cleaved caspase-3), oxidative stress indicators and inflammatory factors in renal tissues were determined. Murine podocyte MPC5 cells were stimulated by high glucose (HG) and transfected with sh-MALAT1 or let-7f mimic, then the cell migration, adhesion ability and apoptosis were evaluated. Moreover, the binding relationship between MALAT1 and let-7f, and the targeting relationship between let-7f and krüppel-like factor 5 (KLF5) were confirmed. Silenced MALAT1 could improve baseline indicators of DN mice, and also improved pathology, increased nephrin and podocin expression, decreased desmin and Cleaved caspase-3 expression, and restrained oxidative stress and inflammatory reaction in their renal tissues. Additionally, elevated let-7f and reduced MALAT1 could restrict migration and apoptosis of HG-induced MPC5 cells, and promoted the cell adhesion ability. Results in our research indicated that the reduced MALAT1 could relieve the podocyte injury in DN by upregulating let-7f and inhibiting KLF5, which may be helpful for DN therapy.
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