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Cardiac response to thromboxane-prostanoid receptor antagonism in a mouse model of muscular dystrophy

ABSTRACT: Cardiac response to thromboxane-prostanoid receptor antagonism in a mouse model of muscular dystrophy

PROVIDER: PRJNA493798 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7940150_1.fastq.gz	Fastqsanger.gz
	SRR7940150_2.fastq.gz	Fastqsanger.gz
	SRR7940151_1.fastq.gz	Fastqsanger.gz
	SRR7940151_2.fastq.gz	Fastqsanger.gz
	SRR7940143_1.fastq.gz	Fastqsanger.gz

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Cardiac response to thromboxane-prostanoid receptor antagonism in a mouse model of muscular dystrophy

Project description:Expression analysis of left ventricle taken from wildtype or delta-sarcoglycan knockout mice, a model of muscular dystrophy. Mice were treated from weaning with vehicle or the thromboxane-prostanoid (TP) receptor antagonist ifetroban. Results provide insight into effects of TP receptor antagonism on cardiomyopathy of muscular dystrophy.

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Project description:Heart failure is the major cause of death for muscular dystrophy patients; however, the molecular pathomechanism remains unknown. Here, we show the detailed molecular pathogenesis of muscular dystrophy-associated cardiomyopathy in mice lacking the fukutin gene (Fktn), the causative gene for Fukuyama muscular dystrophy. Although cardiac Fktn elimination markedly reduced alpha-dystroglycan glycosylation and dystrophin-glycoprotein complex proteins in sarcolemma at all developmental stages, cardiac dysfunction was observed only in later adulthood, suggesting that membrane fragility is not the sole etiology of cardiac dysfunction. During young adulthood, Fktn-deficient mice were vulnerable to pathological hypertrophic stress with downregulation of Akt and the MEF2-histone deacetylase axis. Acute Fktn elimination caused severe cardiac dysfunction and accelerated mortality with myocyte contractile dysfunction and disordered Golgi-microtubule networks, which were ameliorated with colchicine treatment. These data reveal fukutin is crucial for maintaining myocyte physiology to prevent heart failure, and thus, the results may lead to strategies for therapeutic intervention.

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