Objective To explore the effect of microRNA-132 of heart failure and provide theoretical guidance for clinical treatment of heart failure (HF). Methods Peripheral blood was collected from HF patients. RT-qPCR was used to determine microRNA-132 expression. Mouse models of heart failure were established. Color Doppler ultrasound was utilized to measure the changes of cardiac function. HE and Masson staining were applied to observe pathological changes of the myocardium. After H9C2 cells were transfected with microRNA-132, MTT assay was employed to detect the stability of H9C2 cells. ELISA was used to measure the levels of oxidative stress factors. Western blot assay and RT-qPCR were utilized to determine the expression of Bax, Bcl-2, TGF-β1, and smad3. Results MicroRNA-132 expression was downregulated in HF patients' blood. After establishing mouse models of HF, cardiac function obviously decreased. HE staining revealed the obvious edema and hypertrophy of cardiomyocytes. Masson staining demonstrated that cardiomyocytes were markedly fibrotic. After microRNA-132 transfection and H9C2 cell apoptosis induced by H2O2, antioxidant stress and antiapoptotic ability of the H9C2 cells obviously increased. TGF-β1 and smad3 expression remarkably diminished. Conclusion Overexpression of microRNA-132 dramatically increased the antioxidant stress and antiapoptotic ability of H9C2 cells and decreased the expression of TGF-β1 and smad3.

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Microsomal transfer protein (MTP), a lipid transfer protein localized in the endoplasmic reticulum of hepatocytes and enterocytes, plays an important role in the development of nonalcoholic fatty liver disease (NAFLD). Many existing studies have demonstrated that a common polymorphism (-493G>T, rs1800591 G>T) in the MTP gene may be implicated in the development and progression of NAFLD, but individually published results are inconclusive. This meta-analysis aimed to investigate whether MTP -493G>T polymorphism may be a potential risk factor for NAFLD. We searched CISCOM, CINAHL, Web of Science, PubMed, Google Scholar, EBSCO, Cochrane Library, and CBM databases from inception through October 1, 2013. Meta-analysis was performed using the STATA 12.0 software. Eleven clinical case-control studies with a total of 636 NAFLD cases and 918 healthy controls met the inclusion criteria. Our meta-analysis results revealed that MTP -493G>T polymorphism was strongly correlated with an increased risk of NAFLD. Subgroup analysis by ethnicity suggested that MTP -493G>T polymorphism might increase individuals' susceptibility to NAFLD among both Caucasian and non-Caucasian populations. No publication bias was observed in this meta-analysis. In short, the present meta-analysis indicates that MTP -493G>T polymorphisms may contribute to individuals' susceptibility to NAFLD. Thus, MTP -493G>T polymorphism may be a valuable and practical biomarker for early detection of NAFLD.

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ABSTRACT. In this study, we evaluated the associations between the V4 (rs2787094 G>C) polymorphism in a disintegrin and metalloproteinase domain 33 (ADAM33) gene and asthma risk. We searched Web of Science, PubMed, Google Scholar, EBSCO, Cochrane Library, and CBM databases from inception through August 2013, without language restrictions. Meta-analysis was performed using the STATA 12.0 software. Crude odds ratios and 95% confidence intervals were calculated. Eight case-control studies were included, with a total of 2128 asthma patients and 3134 healthy controls. Our results suggest that the ADAM33 V4 polymorphism increases the risk of asthma. Subgroup analysis according to the source of controls revealed significant associations between the ADAM33 V4 polymorphism and risk of asthma in population-and hospital-based subgroups under allele and dominant models (all P < 0.05). Further subgroup analysis using the genotyping method suggested that the ADAM33 V4 polymorphism is correlated with asthma risk in the polymerase chain reaction-restriction fragment length polymorphism subgroup. However, no association was found in the non-polymerase chain reaction-restriction fragment length polymorphism subgroup. Meta-regression analyses showed that the genotyping method may be a main source of heterogeneity (P = 0.003). Our meta-analysis suggests that the ADAM33 V4 polymorphism contributes to the risk of asthma and may be utilized as a biomarker for the early diagnosis of asthma.