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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 age-matched 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 wild-type 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.

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.