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

Figure 5

PTPN4 is the potential target of miR-181c-5p. Overexpression of miR-181c-5p results in reduced levels of protein expression (a) of PTPN4 in H9C2 cardiomyocytes. (b) mRNA and (c) protein expression in H9C2 cardiomyocytes with or without H/R stimulation. (d) mRNA and (e) protein expression in H9C2 cardiomyocytes with or without LPS stimulation. (f) mRNA and (g) protein expression in the postischemic myocardium of rat. Representative Western blots of PTPN4 and GAPDH in the miR-181c-5p agomir (h) or antagomir (i)-transfected H9C2 cardiomyocytes with or without H/R stimulation. Protein presence of PTPN4 was normalized to β-tubulin or GAPDH. mRNA levels are expressed as fold changes against the mRNA expression in H9C2 cardiomyocytes with no stimulation or myocardium in Sham group. Anti-NC: negative control of miR-181c-5p antagomir; data are shown as ; vs. NC agomir (NC) vs. CTL or vs. Sham or vs. CTL-NC agomir (NC) or vs. CTL-NC antagomir (anti-NC), ^# vs. H/R-NC or vs. H/R- anti-NC (two-tailed unpaired Student’s -test in (a–g) and two-way ANOVA followed by Bonferroni test in (h, i)), .