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

Figure 3

Inhibition of miR-181c-5p suppressed NFκB-mediated inflammation in H9C2 cardiomyocytes in response to H/R stimulation. Inhibition of miR-181c-5p attenuated the H/R-induced LDH release (a). (b) 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 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. (c) mRNA expression of NFκB-dependent genes, including IL-1β, IL-6, and TNFα in the anti-NC- or anti-miR-181c-5p-transfected H9C2 cardiomyocytes with H/R stimulation. mRNA levels are expressed as fold changes against those mRNA expressions in anti-NC-transfected H9C2 cardiomyocytes with no stimulation. Anti-NC: negative control of miR-181c-5p antagomir; data are shown as ; vs. CTL, ^# vs. NC antagomir (anti-NC) (two-way ANOVA followed by Bonferroni test in (a–c) and two-tailed unpaired Student’s -test in (d)), .

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