MicroRNA­198 contributes to lupus nephritis progression by inhibition of phosphatase and tensin homology deleted on chromosome ten expression.

ABSTRACT

A number of short noncoding microRNAs (miRs) have been demonstrated to be highly expressed in many kidney diseases such as renal cancer and lupus nephritis (LN); however, these results have not been extensively investigated. The aim of the present study was to investigate the expression and function of miR­198 in LN based on the previous studies. miR­198 expression level in systemic lupus erythematosus (SLE) patients was determined to determine its clinicopathological significance and effect on glomerular cell proliferation. It was demonstrated that higher expression of miR­198 was observed in patients with SLE, and was correlated with disease activity. Bioinformatics prediction and luciferase assays were used to demonstrate that miR­198 could directly bind to the phosphatase and tensin homology deleted on chromosome ten (PTEN) 3'­untranslated region. Furthermore, miR­198 overexpression reduced PTEN expression levels, while miR­198 silencing increased its expression at both the mRNA and protein level. Furthermore, there was a negative association between miR­198 and PTEN in the patients with active SLE. Thus, miR­198 may promote proliferation and contribute to SLE progression by targeting PTEN.