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Reactive oxygen species (ROS) induced oxidative stress leads to cell damage and neurological disorders in astrocytes. The gap junction protein connexin43 (Cx43) could form intercellular channels in astrocytes and the expression of Cx43 plays an important role in protecting the cells from damage. In the present study, we investigated the contribution of Cx43 to astrocytic necrosis induced by the ROS hydrogen peroxide (H2O2) and the mechanism by which AMPK was involved in this process. Fluorescence microscopy, flow cytometry, and western blot were used quantitatively and qualitatively to determine the cell apoptosis, necrosis, and protein expression. Lack of Cx43 expression or blockage of Cx43 channels resulted in increased H2O2-induced astrocytic necrosis, supporting a cell protective effect of functional Cx43 channels. Our data suggest that AMPK is important for Cx43-mediated ROS resistance. Inhibition of AMPK activation results in reduction of necrosis and ROS production. Taken together, our findings suggest that the role of Cx43 in response to H2O2 stress is dependent on the activation of AMPK signaling pathways and regulates ROS production and cell necrosis.

MicroRNAs are widely involved in cancer progression by inhibiting the expression levels of oncogenes or tumor suppressor genes, and dysregulation of microRNAs may contribute to tumorigenesis. Here, we found that overexpressed miR-208b can reduce the proliferation of human osteosarcoma cell lines U-2OS and Saos-2 by arresting cell cycle progression. The in vivo xenograft tumors induced by Saos-2 cells overexpressing miR-208b had smaller size and grew more slowly than those induced by the control cells. The mobility of U-2OS or Saos-2 cells was also downregulated by miR-208b. MiR-208b targeted a site in the 3' untranslated region of receptor tyrosine kinase-like orphan receptor 2. Inhibition of receptor tyrosine kinase-like orphan receptor 2 suppresses osteosarcoma metastasis in vitro. Recovering the expression levels of receptor tyrosine kinase-like orphan receptor 2 in miR-208b-overexpressed U-2OS or Saos-2 cells attenuated the inhibitory effects of miR-208b. In addition, the expression levels of miR-208b are significantly reduced in human osteosarcoma tissue samples compared to normal tissue samples, and miR-208b levels correlated inversely with receptor tyrosine kinase-like orphan receptor 2 levels. On these bases, we identified that miR-208b targets receptor tyrosine kinase-like orphan receptor 2 gene by which miR-208b can regulate the development of osteosarcoma.

OBJECTIVESThis study aims to compare the prevalence of metabolic syndrome between Korean emigrants (KEs) and their host country residents in Japan and China.METHODSThe Korean Emigrant Study (KES) is a cohort study initiated in 2005 to elucidate the effect of genetic susceptibility and environmental change on hypertension, diabetes, and metabolic syndrome. Equal numbers of KEs and host country residents, aged 30 or over, were recruited from three regions; Kobe-Osaka in Japan (total number=965), Yanbian in China (n=1,019), and Changchun in China (n=949).RESULTSThe age-adjusted prevalences of metabolic syndrome among KEs in Kobe-Osaka were significantly higher than those among Japanese (in men 24.0% vs. 15.6%, p=0.04, in women 8.4% vs. 2.7%, p=0.01), while the age-adjusted prevalences among KEs in Changchun were similar to those among Chinese (in men 11.7% vs. 16.1%, p=0.37, in women 28.3% vs. 30.1%, p=0.91). The age-adjusted prevalences were generally higher in Yanbian than other regions, and KEs had higher prevalence than Chinese in men but not in women (in men 37.9% vs. 28.3%, p=0.03, women 46.0% vs. 50.6%, p=0.44). The components with significant ethnic differences in prevalence were high blood pressure and abdominal obesity in Japan, and triglyceride in China. The most influential component in diagnosing metabolic syndrome was abdominal obesity in men and triglyceride in women.CONCLUSIONThe prevalence of metabolic syndrome was higher in KEs than in host country residents in Japan but not in China. Abdominal obesity and triglyceride are both discriminating and influential components in metabolic syndrome.