Research Paper Volume 13, Issue 7 pp 10158—10174

Hypoxia-induced miR-27 and miR-195 regulate ATP consumption, viability, and metabolism of rat cardiomyocytes by targeting PPARγ and FASN expression

Inhibition of miR-27 and miR-195 regulated hypoxia-affected mitochondrial metabolism and ATP consumption. Isolated cardiomyocytes were transfected with NC, miR-27, and miR-195 inhibitors for 24 h followed by hypoxia treatment for 24 h. Cells under normoxia served as controls. (A) ATP consumption of cells in each group. (B) Glycolysis rates of the cells in each group. (C) Oxidation rates of glucose, palmitate, and lactate of the cells in each group (n = 3). *P #P

Figure 3. Inhibition of miR-27 and miR-195 regulated hypoxia-affected mitochondrial metabolism and ATP consumption. Isolated cardiomyocytes were transfected with NC, miR-27, and miR-195 inhibitors for 24 h followed by hypoxia treatment for 24 h. Cells under normoxia served as controls. (A) ATP consumption of cells in each group. (B) Glycolysis rates of the cells in each group. (C) Oxidation rates of glucose, palmitate, and lactate of the cells in each group (n = 3). *P < 0.05 vs. the normoxia group. #P < 0.05 vs. the hypoxia group.