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 TGF beta and NF-kappa B signaling activation in Ang II-induced podocytes. SMOC2 regulated cell viability, apoptosis and extracellular matrix (ECM) deposition in Ang II-induced podocytes via TGF beta signaling, and SMOC2 regulated inflammation in Ang II-induced podocytes through NF-kappa B signaling. Overall, our study demonstrated that miRNA-17-5p restrained the dysfunction of Ang-II induced podocytes by suppressing SMOC2 via the NF-kappa B and TGF beta signaling.

Automated summary

This study revealed that miR-17-5p regulates Ang II-induced podocyte injury by suppressing SMOC2 through NF-kappa B and TGF beta signaling pathways.