MiR-922 alleviates LPS-induced HK-2 cell apoptosis and inflammation through TGF-β/Smad

MicroRNAs play an extensive role in human chronic kidney diseases (CKD), but the role of miR-922 remains unclear.

This study was designed to investigate the potential mechanism by which miR-922 acts in CKD.

The human proximal renal tubular cell line (HK-2) was treated by LPS to build a CKD cell model. The expressions of miR-922, TGFβR1, and p-Smad2/3 were detected by RT-qPCR or western blotting. The dual-luciferase reporter assay verified the interaction of miR-922 with TGFβR1. Cell viability and apoptosis were assessed using the CCK-8 assay and Annexin V-FITC/PI method. An ELISA kit was used for the measure of TNF-α/IL-1β levels.

MiR-922 was scanty in HK-2 cells with LPS treatment. MiR-922 was an upstream regulator of TGFβR1. The up-regulation of miR-922 restrained TGFβR1 expression, thereby hindering the activation of Smad2/3. Overexpression of miR-922 and inhibition of Smad2/3 alleviated the LPS-induced apoptosis and inflammation, while TGFβR1 played a pro-apoptotic and pro-inflammatory role.

MiR-922 rescued HK-2 cell apoptosis and inflammation damage induced by LPS through negative regulation of TGF-β/Smad pathway, which may be a vital molecular mechanism of CKD.