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

Figure 2

Overexpression of miR-181c-5p exacerbated NFκB-mediated inflammation in H9C2 cardiomyocytes in response to H/R stimulation. miR-181c-5p agomir (miR-181c-5p) transfection resulted in significant overexpression of miR-181c-5p in H9C2 cardiomyocytes (a), and overexpression of miR-181c-5p exacerbated the H/R-induced LDH release (b). (c) 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 H/R stimulation. Protein presence of phosphorylated IκBα (Ser^32/36), IκBα, and phosphorylated p65 (Ser⁵²⁶) was normalized to IκBα, β-tubulin, and p65, respectively. (d) mRNA expression of NFκB-dependent genes, including IL-1β, IL-6, and TNFα in the NC- or miR-181c-5p agomir-transfected H9C2 cardiomyocytes with H/R stimulation. mRNA levels are expressed as fold changes against those mRNA expressions in NC-transfected H9C2 cardiomyocytes with no stimulation. Data are shown as ; vs. CTL, ^# vs. NC agomir (NC) (two-tailed unpaired Student’s -test in (a, d) and two-way ANOVA followed by Bonferroni test in (b, c)), .

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