Molecular mechanism and role of miRNA-155 ribonucleic acid in podocyte apoptosis in lupus nephritis: SOCS1 protein expression regulates JAK/STAT pathway transduction

This study aimed to explore the specific role of miRNA-155 in the process of podocyte apoptosis within the context of lupus nephritis, as well as to elucidate the underlying molecular mechanisms through which miRNA-155 exerts its effects, particularly focusing on the SOCS1/JAK1-STAT1 signaling pathway. To investigate the direct influence of miRNA-155 on podocyte apoptosis, the researchers employed a cultured glomerular podocyte system, in which they transfected these cells with either mimics of miRNA-155 or inhibitors. The subsequent effects on podocyte apoptosis were carefully monitored. Additionally, various methodologies including Western blot analysis, immunofluorescence, and flow cytometry were utilized to assess the expression levels and phosphorylation states of key proteins involved in the SOCS1/JAK1-STAT1 pathway, aiming to determine their roles in the apoptosis mediated by miRNA-155.A dual luciferase reporter assay was conducted to confirm the direct interaction between miRNA-155 and the mRNA of SOCS1. The findings of the study indicated a significant increase in miRNA-155 expression, which was positively correlated with the podocyte apoptosis index, suggesting that higher levels of miRNA-155 were linked to increased cell death. Investigating the underlying mechanism, the study revealed that miRNA-155 promotes podocyte apoptosis by activating the JAK1-STAT1 signaling pathway through the downregulation of SOCS1 protein levels. The dual luciferase reporter gene assay provided further validation of the hypothesis that miRNA-155 directly targets the 3' untranslated region of SOCS1 mRNA, thereby inhibiting its expression and facilitating the apoptotic process in podocytes.