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Fig. 7 | Clinical Epigenetics

Fig. 7

From: Abnormal expression of PRKAG2-AS results in dysfunction of cardiomyocytes through regulating PRKAG2 transcription by interacting with PPARG

Fig. 7

Up-regulation of PRKAG2-AS may result in abnormal heart function. A Analysis of the GSE4172 dataset showed elevated expression of PRKAG2-AS in the myocardium of patients with inflammatory dilated heart failure. B PRKAG2-AS expression was significantly up-regulated in DCM heart samples collected for this study. C Overexpression of PRKAG2-AS in AC16 cells was achieved by adenovirus. D-E Overexpression of PRKAG2-AS increased the expression of PRKAG2b and PRKAG2d. F-G The expression of PRKAG2b and PRKAG2d was significantly elevated in DCM heart samples compared to control hearts. H There was a positive correlation between the expression of PRKAG2-AS and that of PRKAG2b and PRKAG2d in heart failure. I Overexpression of PRKAG2-AS increased the expression of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and Ī²-myosin heavy chain (Myh7) while decreasing the expression level of the Ī±-myosin heavy chain (Myh6) in AC16 cardiomyocytes. J Knockdown of PRKAG2-AS in cardiomyocytes decreased the expression of ANP, BNP, and Myh7

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