Mouse Anti Human Glutathione S-transferase Mu1 Hybridoma [DQUD-HTUNv2-3]

Background:A meta-analysis was applied to evaluate the associations between the glutathione-S-transferases (GSTs) M1/T1 gene polymorphisms and male infertility in Chinese populations.Methods:A comprehensive search for articles was conducted from PubMed, Web of Science, Embase, China biology medical literature database (CBM), China National Knowledge Infrastructure (CNKI), VIP, and Chinese literature database(Wang fang) up to April 30, 2018. All of the statistical analyses were performed using Review Manager 5.3 and Stata 14.0.Results:Ten studies on GSTM1 gene polymorphism involving 3302 cases and 1959 controls, and ten studies on GSTT1 gene polymorphism involving 3048 cases and 1861 controls were included in this meta-analysis. Overall, the null genotype of GSTM1/GSTT1 was significantly related to male infertility risk in Chinese populations (GSTM1, OR=1.35, 95% CI: 1.02-1.78; GSTT1, OR=1.40, 95% CI: 1.15-1.70). In subgroup analyses stratified by infertility type, significant association was observed between GSTT1 null genotype and male infertility in both nonobstructive azoospermia (NOA) and oligoasthenozoospermia (OAT). However, the GSTM1 null genotype was associated with OAT, but not NOA in Chinese populations. The sensitivity analysis confirmed the reliability and stability of the meta-analysis.Conclusion:Our meta-analysis supports that the GSTM1/GSTT1 null genotype might contribute to individual susceptibility to male infertility in Chinese populations.

This study aimed to investigate the roles of RPSAP52 in renal failure. Our results showed that RPSAP52 was upregulated in plasma of renal failure patients in comparison to healthy controls. Dual luciferase reporter assay showed that RPSAP52 could interact with miR-423-5p, while overexpression of RPSAP52 and miR-423-5p did not alter the expression of each other in human renal proximal tubular epithelial cells (HRPTEpCs). In addition, overexpression of RPSAP52 increased the expression levels of GSTM1 in HRPTEpCs. Cell apoptosis assay showed that overexpression of RPSAP52 and GSTM1 decreased the apoptotic rate of HRPTEpCs under hypoxia conditions. MiR-423-5p played an opposite role and attenuated the effects of overexpressing RPSAP52 and GSTM1. Therefore, RPSAP52 may regulate miR-423-5p/GSTM1 axis to suppress hypoxia-induced HRPTEpC apoptosis.