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OBJECTIVE: To elucidate how microRNA-27a and FoxO1 regulate cardiac dysfunction in mice. MATERIALS AND METHODS: Expression levels of ANP, BNP, β-MHC, α-SMA, Fn1, and Periostin in myocardial tissues of 2-month-old and 8-month-old microRNA-27a-KO mice and agematched wild-type mice were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot. Dual-luciferase reporter gene assay was conducted in H9C2 cells to verify the binding condition between microRNA-27a and FoxO1. By transfection of microRNA-27a mimics or inhibitor, FoxO1 expression in H9C2 cells was determined at the mRNA and protein levels. HW/BW [ratio of heart weight (mg) and body weight (mg)], HW/ TL [ratio of heart weight (mg) and tibial length (mm)], LVPWDT [left ventricular posterior wall diastolic thickness (mm)], LVEDD [left ventricular end-diastolic dimension (mm)], and FS (fractional shortening) in mice treated with or without FoxO1 inhibitor AS1842856 were accessed through echocardiography. RESULTS: MicroRNA-27a-KO mice had larger LVEDD, HW/BW, and HW/TL, but lower FS and LVPWDT than those of age-matched wildtype mice. Besides, higher levels of ANP, BNP, β-MHC, α-SMA, Fn1, and Periostin were observed in myocardial tissues of microRNA-27a-KO mice compared with those of age-matched wild-type mice. Dual-luciferase reporter gene assay revealed lower luciferase activity in H9C2 cells co-transfected with microRNA-27a mimics and wild-type FoxO1 than that of controls. The expression level of FoxO1 was negatively regulated by microRNA-27a in H9C2 cells at the mRNA and protein levels. After AS1842856 injection, HW/BW, HW/TL, and LVEDD in microRNA- 27a-KO mice markedly decreased, whereas FS and LVPWDT elevated. By comparison, AS1842856 injection did not influence cardiac development in wild-type mice. CONCLUSIONS: MicroRNA-27a knockout could induce cardiac dysfunction in mice through upregulating FoxO1 expression. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This study aims to explore the expression of micro-ribonucleic acid (miRNA)-210 in the cerebral cortex of rat model with global cerebral ischemia, and determine its function on the regulation of the apoptosis of neuronal cells. MATERIALS AND METHODS: Rat models of global cerebral ischemia were established in vitro. Rats were euthanized at 24 h after reperfusion and the cerebral cortex was collected. The expression of miRNA-210 was detected by reverse transcription- quantitative polymerase chain reaction (RT-qPCR). Neuronal cells were transfected by liposomes in vitro and cells were divided into neuronal cell group (group i), neuronal cell + miRNA- 210 mimic group (group ii) and neuronal cell + miRNA-210 inhibitor group (group iii). The cell apoptosis rate and gene and protein expressions of HIF-1α, VEGF and Caspase-3 were measured. RESULTS: The level of miRNA-210 in rats with global cerebral ischemia was remarkably higher than that in rats from sham operation group (p<0.05). The apoptosis rate of neuronal cells was increased evidently when miRNA-210 was overexpressed, and the expressions of HIF-1α, VEGF and Caspase-3 were elevated markedly at both mRNA and protein levels. CONCLUSIONS: Our data indicate that miRNA- 210 expression is upregulated in the rats with global cerebral ischemia, and the rise of miRNA-210 level increases the apoptosis of neuronal cells through the activation of HIF-1α- VEGF signaling pathway. [ABSTRACT FROM AUTHOR]

To evaluate the potential effect of interaction between breastfeeding and environmental tobacco smoke ( ETS) exposure on respiratory health, we studied 31 049 children (aged 2-14 years) from 25 districts of seven cities in northeast China. Parents of the children completed standardized questionnaires that characterized the children's histories of respiratory symptoms and illness, feeding methods, ETS exposure, and other associated risk factors. Breastfeeding was defined as having been mainly breastfed for 3 months or more. The results showed that the association of ETS exposure with childhood respiratory conditions/diseases was modified by breastfeeding, and the association for nonbreastfed children was stronger than that for breastfed children. In particular, for nonbreastfed children, the odds ratios ( ORs) for the effect of current ETS exposure asthma was 1.71 (95% CI: 1.43-2.05); however, the OR for breastfed children was 1.33 (95% CI: 1.20-1.48), indicating that the interactions between breastfeeding and current ETS exposure on asthma were statistically significant ( P = 0.019). When stratified by school (kindergarten vs. elementary school), breastfeeding was more protective for asthma-related symptoms among children from kindergarten. In conclusion, this study shows that breastfeeding is associated with smaller associations between ETS exposure and respiratory conditions in children, suggesting that breastfeeding reduces susceptibility to the respiratory effects of ETS. [ABSTRACT FROM AUTHOR]

HeLa cells were exposed to formaldehyde and its metabolic derivatives, methanol, formic acid, and acetaldehyde, to investigate that the toxicity of formaldehyde is not caused by the chemical group. After 1 h of treatment with formaldehyde, mitochondrial assays showed that low concentrations (e.g. 10 μmol/L) of formaldehyde promoted growth of the HeLa cells, while higher concentrations (e.g. ≥62.5 μmol/L) inhibited cell growth; while all four chemicals at a concentration of 125 μmol/L affected cell growth, formaldehyde affected the largest. Reactive oxygen species concentration increased with the concentration of the exposure chemical. The endogenous formaldehyde content increased the most in the formaldehyde group, but in other three groups, it did not increase as the exposure concentration increased. Expression of dehydrogenase (formaldehyde dehydrogenase (FDH)) in the formaldehyde (10.40) and methanol (10.60) groups increased significantly compared with the control (1), while it was similar to the control in formic acid (0.90) and acetaldehyde (1.10) groups. Our results suggest that formaldehyde could affect cell activity and even enter cells. Exposure to formaldehyde changes the endogenous formaldehyde concentration in cells within 24 h, and this induces expression of FDH for formaldehyde degradation to maintain the formaldehyde balance. The toxicity of formaldehyde is not caused by the carbon atoms in the aldehyde, hydroxyl, or carboxyl groups. Formaldehyde is hypothesized to be an important signaling molecule in the regulation of cell growth and maintenance of the endogenous formaldehyde level., (© The Author(s) 2014.)