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

Figure 4

miR-181c-5p exacerbated LPS-induced NFκB signalling in H9C2 cardiomyocytes. Increased expression of miR-181c-5p in lipopolysaccharide (LPS, 3 μg/ml, 21 h) stimulated H9C2 cardiomyocytes (a). (b) Representative Western blots of phosphorylated IκBα (Ser^32/36), IκBα, phosphorylated p65 (Ser⁵²⁶), p65, and β-tubulin in the NC- or miR-181c-5p agomir-transfected H9C2 cardiomyocytes with or without LPS stimulation. (c) Representative Western blots of phosphorylated IκBα (Ser^32/36), IκBα, phosphorylated p65 (Ser⁵²⁶), p65, and β-tubulin in the anti-NC- or miR-181c-5p antagomir (anti-miR-181c-5p)-transfected H9C2 cardiomyocytes with or without LPS stimulation. Protein presence of phosphorylated IκBα (Ser^32/36), IκBα, and phosphorylated p65 (Ser⁵²⁶) was normalized to IκBα, β-tubulin, and p65, respectively. Anti-NC: negative control of miR-181c-5p antagomir; data are shown as ; vs. CTL, ^# vs. NC agomir (NC) or NC antagomir (anti-NC) (two-tailed unpaired Student’s -test in (a) and two-way ANOVA followed by Bonferroni test in (b, c), .