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Fig. 3 | Clinical Epigenetics

Fig. 3

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

Fig. 3

Knockdown of PRKAG2-AS-induced apoptosis of cardiomyocytes. A-B Apoptosis or necrosis of cardiomyocytes was not significantly increased after cytoplasmic PRKAG2-AS was knocked down by siRNA compared to NC controls. C-D Knockdown of nuclear PRKAG2-AS by antisense oligos led to a significant increase in apoptosis of cardiomyocytes. E Analysis of SOD1, SOD2, and SOD3 expression in the hypoxic cardiomyocyte model revealed that SOD1 and SOD3 were down-regulated by hypoxia. F Cytoplasmic knockdown of PRKAG2-AS by siRNA decreased the expression level of SOD1 but did not affect the expression of SOD2 and SOD3. G Nuclear knockdown of PRKAG2-AS reduced the expression of SOD1 and SOD3 in cardiomyocytes

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Clinical Epigenetics

ISSN: 1868-7083

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