Fig. 8From: Abnormal expression of PRKAG2-AS results in dysfunction of cardiomyocytes through regulating PRKAG2 transcription by interacting with PPARGElevated expression of PRKAG2b and PRKAG2d leads to abnormal heart function. A Western blot confirms elevated PRKAG2 expression in primary cardiomyocytes transfected with PRKAG2b adenovirus at 10 MOI and 50 MOI. BāE Overexpression of PRKAG2 increases the expression of ANP, BNP, and Myh7. F Overexpression of PRKAG2 significantly increases cardiomyocyte sizes. GāK Knockdown of PRKAG2b and PRKAG2d reduces the expression levels of ANP, BNP, Myh7, and Myh6 in normal cultured cardiomyocytes and attenuates PE-induced up-regulation of ANP and BNP in a hypertrophic cardiomyocyte model. (L) Knockdown of PRKAG2b and PRKAG2d reduces PE-induced enlargement of cardiomyocyte sizeBack to article page