Effects of miR-151-3p-mediated GLCCl1 expression on biological function in children with nephrotic syndrome

This study aimed to confirm the association of miR-151-3p with nephrotic syndrome (NS) in children and to explore the molecular mechanisms by which glucocorticoid-induced transcript 1 gene (GLCCI1) targets cellular biological functions in children with nephrotic syndrome.

miR-151-3p levels were detected in 20 children with hormone-sensitive nephrotic syndrome (SSNS), 15 children with steroid-dependent nephrotic syndrome (SDNS) and 20 children with steroid-resistant nephrotic syndrome (SRNS), using qRT-PCR before and after glucocorticoid treatment, and TargetScan information software was used to predict the biological targets between miR-151-3p and GLCCI1 gene. The change in albumin-to-creatinine ratio (ACR) before and after treatment in children with NS was determined to judge the treatment efficacy.

Compared with healthy controls, pediatric patients with NS had significantly increased serum miR-151-3p levels before treatment (P<0.01). After glucocorticoid treatment, children with SSNS/SDNS had significantly decreased serum miR-151-3p levels (P<0.01), with no significant difference from healthy controls. The ACR of children with SSNS/SDNS was significantly lower than that before treatment (P<0.05), and the symptoms of proteinuria were significantly relieved. The serum miR-151-3p levels and ACR of children with SRNS did not change significantly from that before treatment (P>0.05), and the symptoms of proteinuria were also not improved. Targetscan prediction results showed that miR-151-3p has well-matched sites with GLCCI13'UTR.

miR-151-3p directly influences the onset and progression of NS through targeted regulation of GLCCI1 expression in podocytes. miR-151-3p may be a biological marker for the diagnosis, treatment and prognosis of NS.