Figure 3.

Nickel-induced miR-210 expression modulates the shift of energy metabolism. (a) Cell viability was determined by the CCK8 assay after nickel treatment. The inhibitors of glycolysis, 2-DG (10 mM) or BrPA (25 μM), exacerbate the cytotoxicity of nickel. (b) A representative oxygen consumption curve that bases on the real-time detected partial pressure of oxygen (mmHg) surrounding the cells indicates the suppression of nickel on cellular oxygen consumption. (c) Transfection of miR-210 mimic reduces the oxygen consumption rate (OCR) of cells in non-NiCl₂ conditions, and inhibition of miR-210 eases off the repression of oxygen consumption rate caused by nickel exposure. (d) The transfection of miR-210 mimic reduces the concentration of cellular ATP in non-NiCl₂ conditions, and inhibition of miR-210 attenuates the ATP depletion caused by nickel exposure. (e) The activity of hexokinase (HK) was measured based on the coupled reactions of HK and 6-phosphoglucose dehydrogenase and reflected by the change of optical density at 340 nm (ΔmOD₃₄₀/min/mg) measuring the generation of NADPH. The transfection of miR-210 mimic enhances the activity of HK in non-NiCl₂ conditions, and inhibition of miR-210 mitigates the HK activity increase caused by nickel exposure. (f) The transfection of miR-210 mimic increases the content of cellular lactic acid in non-NiCl₂ conditions, and inhibition of miR-210 attenuates the lactic acid accumulation caused by nickel exposure. The abbreviations M, MC, I, and IC indicate the transfection of miR-210 mimic, mimic-control, miR-210 inhibitor, and inhibitor-control, respectively. The sign ‘+' indicates the treatment of 1 mM NiCl₂ for 4 h, and the sign ‘−' indicates the corresponding sham treatment. The error bar reflects the S.E.M. of at least three independent experiments. *P<0.05 compared with the control