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Excessive O-GlcNAcylation causes heart failure and sudden death

ABSTRACT: Excessive O-GlcNAcylation causes heart failure and sudden death

PROVIDER: PRJNA553816 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9668830_1.fastq.gz	Fastqsanger.gz
	SRR9668830_2.fastq.gz	Fastqsanger.gz
	SRR9668840_1.fastq.gz	Fastqsanger.gz
	SRR9668840_2.fastq.gz	Fastqsanger.gz
	SRR9668850_1.fastq.gz	Fastqsanger.gz

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Excessive O-GlcNAcylation causes heart failure and sudden death

Project description:Heart failure is a leading cause of death worldwide, and failing heart muscle is marked by increased O-GlcNAcylation (OGN). It is unknown if excessive OGN contributes to cardiomyopathy and heart failure. OGN modifies serines and threonines, total OGN levels follow cellular nutrient and metabolic flux in addition to net activity of O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA). We developed new transgenic mouse models with myocardial delimited over-expression of OGA and OGT, and found that OGT transgenic mice developed severe cardiomyopathy and premature death. In contrast, OGA transgenic hearts had normal function, but were resistant to pathological stress. Interbreeding OGA transgenic mice rescued cardiomyopathy and premature death in OGT transgenic mice. RNA Seq and functional studies highlighted disrupted metabolism in hearts from OGT transgenic mice that was rescued by OGA transgenic interbreeding. Here we show excessive OGN causes cardiomyopathy, identify gene programs responsive to pathological OGN, and suggest attenuation of OGN may be an effective therapy for heart failure.

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Project description:Sudden cardiac death (SCD) in patients with heart failure (HF) is allied with an imbalance in reduction-oxidation (redox) signaling in cardiomyocytes; however, the basic pathways and mechanisms governing redox homeostasis in cardiomyocytes are not fully understood. Here, we show that cytochrome b5 reductase 3 (CYB5R3), an enzyme known to regulate redox signaling in erythrocytes and vascular cells, is essential for cardiomyocyte function. Using a conditional cardiomyocyte-specific CYB5R3 knockout mouse, we discovered that deletion of CYB5R3 in male adult cardiomyocytes, but not female, causes cardiac hypertrophy, bradycardia, and SCD. The increase in SCD in CYB5R3 KO mice is associated with calcium mishandling, ventricular fibrillation, and cardiomyocyte hypertrophy. Molecular studies reveal that CYB5R3 KO hearts display decreased ATP, increased oxidative stress, suppressed coenzyme Q levels, and hemoprotein dysregulation. Lastly, from a translational perspective, we reveal that the high-frequency missense genetic variant rs1800457, which translates into a CYB5R3 T117S partial loss-of-function protein, associates with decreased event-free survival (~20%) in African Americans with HF with reduced ejection fraction (HFrEF). Together, these studies reveal a crucial role for CYB5R3 in cardiomyocyte redox biology and identify a new genetic biomarker for individuals in the African American population that may potentially increase the risk of death from HFrEF.

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