MiR-181c-5p Promotes Inflammatory Response during Hypoxia/Reoxygenation Injury by Downregulating Protein Tyrosine Phosphatase Nonreceptor Type 4 in H9C2 Cardiomyocytes

Figure 1

miR-181c-5p was upregulated concomitantly with enhanced NFκB activity in posthypoxic H9C2 cardiomyocytes and postischemic myocardium of rat. (a) Increased expression of miR-181c-5p in hypoxia/reoxygenation (H/R, 6 h hypoxia followed by 6 h reoxygenation) stimulated H9C2 cardiomyocytes. (b) Representative Western blots of phosphorylated IκBα (Ser^32/36), IκBα, phosphorylated p65 (Ser⁵²⁶), p65, and β-tubulin in the H/R-stimulated H9C2 cardiomyocytes. In the in vivo model, myocardial I/R (30 minutes of left anterior descending artery occlusion and 2 hours of reperfusion in rats) induced significant increased postischemic myocardial infarction size (c) and upregulation of miR-181c-5p (d). (e) Representative Western blots of phosphorylated IκBα (Ser^32/36), IκBα, phosphorylated p65 (Ser⁵²⁶), p65, and β-tubulin in postischemic myocardium of rat. Protein presence of phosphorylated IκBα (Ser^32/36), IκBα, and phosphorylated p65 (Ser⁵²⁶) was normalized to IκBα, β-tubulin, and p65, respectively. Data are shown as ; vs. CTL or Sham (two-tailed unpaired Student’s -test), .

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