OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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. AJTR
OBJECTIVE: 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. METHODS: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. RESULTS: 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. CONCLUSION: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. AJTR
Authors: Kyle Kai-How Farh; Andrew Grimson; Calvin Jan; Benjamin P Lewis; Wendy K Johnston; Lee P Lim; Christopher B Burge; David P Bartel Journal: Science Date: 2005-11-24 Impact factor: 47.728
Authors: Debbie S Gipson; Susan F Massengill; Lynne Yao; Shashi Nagaraj; William E Smoyer; John D Mahan; Delbert Wigfall; Paul Miles; Leslie Powell; Jen-Jar Lin; Howard Trachtman; Larry A Greenbaum Journal: Pediatrics Date: 2009-07-27 Impact factor: 7.124