MicroRNA‐17‐5p restrains the dysfunction of Ang‐II induced podocytes by suppressing secreted modular calcium‐binding protein 2 via NF‐κB and TGFβ signaling.

Glomerulonephritis, also known as nephritis syndrome (nephritis for short), is a common kidney disease. Previous research has proved that microRNAs (miRNAs) frequently regulate various diseases including nephritis. Nonetheless, the biological function and molecular mechanism of miR‐17‐5p are unclear in nephritis. In the current study, RT‐qPCR analysis showed that miR‐17‐5p was downregulated in Ang II‐induced podocytes. Also, according to the results from RT‐qPCR analysis, CCK‐8 assay, flow cytometric analysis, western blot analysis, and ELISA miR‐17‐5p elevation alleviated Ang II‐induced podocyte injury. Besides, luciferase reporter assay, western blot and RT‐qPCR analyses revealed that SMOC2 was targeted by miR‐17‐5p in Ang II‐induced podocytes. Additionally, rescue assays demonstrated that overexpressed SMOC2 counteracted the influence of overexpressed miR‐17‐5p on cell injury of Ang II‐induced podocytes. Moreover, our data suggested that miR‐17‐5p‐SMOC2 axis regulated TGFβ and NF‐κB signaling activation in Ang II‐induced podocytes. SMOC2 regulated cell viability, apoptosis and extracellular matrix (ECM) deposition in Ang II‐induced podocytes via TGFβ signaling, and SMOC2 regulated inflammation in Ang II‐induced podocytes through NF‐κB signaling. Overall, our study demonstrated that miRNA‐17‐5p restrained the dysfunction of Ang‐II induced podocytes by suppressing SMOC2 via the NF‐κB and TGFβ signaling. [ABSTRACT FROM AUTHOR]