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The effect of Sulfonulyrea short form (SUR2A-55) overexpression on cardiac gene expression

ABSTRACT: The effect of Sulfonulyrea short form (SUR2A-55) overexpression on cardiac gene expression

PROVIDER: PRJNA1026827 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26346282_1.fastq.gz	Fastqsanger.gz
	SRR26346282_2.fastq.gz	Fastqsanger.gz
	SRR26346283_1.fastq.gz	Fastqsanger.gz
	SRR26346283_2.fastq.gz	Fastqsanger.gz
	SRR26346284_1.fastq.gz	Fastqsanger.gz

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The effect of Sulfonulyrea short form (SUR2A-55) overexpression on cardiac gene expression

Project description:The small splice variant of the sulfonylurea receptor protein isoform 2A (SUR2A-55) targets mitochondria and enhances mitoKATP activity. In male mice the overexpression of this protein promotes cardioprotection protecting hearts from ischemia reperfusion injury. However, it is unclear what impact this has on the female myocardium as SUR2A and KATP channels are known to be differentially expressed in male and female hearts. To define the impact of SU2R2A-55 on the female heart, RNA seq was performed on hearts from mice with cardiac specific transgenic overexpression of SUR2A-55 (TGSUR2A-55). RNA seq analysis found 227 differnetial expressed genes between WT and TGSUR2A-55 female mouse hearts that were enriched in pathways of cellular metabolism. This was in direct contrast to male mice that had only three differentially expressed genes. Future research directed at the expression and activity of mitoKATP subunits according to sex may elucidate gender specific treatments.

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Project description:Akt is a serine/threonine protein kinase that is activated by a variety of growth factors or cytokines in a PI3-kinase dependent manner. Using a conditional transgenic system in which Akt signaling can be turned on or off in the adult heart, we have recently demonstrated that short-term Akt activation induces a ‘physiological’ form of cardiac hypertrophy with enhanced coronary angiogenesis and maintained contractility. Here we tested the hypothesis that induction of physiological hypertrophy by short-term Akt activation might improve contractile function in failing hearts. When Akt signaling was transiently activated in murine hearts with impaired contractility induced by pressure overload or adriamycin treatment, contractile dysfunction was attenuated in both cases. Importantly, improvement of contractility was observed before the development of cardiac hypertrophy, indicating that Akt improves contractile dysfunction independently of its growth-promoting effects. To gain mechanistic insights into Akt-mediated positive inotropic effects, transcriptional profiles in the heart were determined in a pressure overload-induced heart failure model. Biological network analysis of differentially expressed transcripts revealed significant alterations in the expression of genes associated with cell death, and these alterations were reversed by short-term Akt activation. Thus, short-term Akt activation improves contractile dysfunction in failing hearts. This beneficial effect of Akt on contractility is hypertrophy-independent and may be mediated in part by inhibition of cell death associated with heart failure. Keywords: transgenic mice, Akt1, cardiac hypertrophy after ascending aortic constriction and contractile dysfunction, DNA microarrays

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