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Circulating miR-499a-5p is a potential biomarker of MYH7-associated hypertrophic cardiomyopathy

ABSTRACT: Circulating miR-499a-5p is a potential biomarker of MYH7-associated hypertrophic cardiomyopathy

PROVIDER: PRJNA800655 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17761264.fastq.gz	Fastqsanger.gz
	SRR17761265.fastq.gz	Fastqsanger.gz
	SRR17761266.fastq.gz	Fastqsanger.gz
	SRR17761267.fastq.gz	Fastqsanger.gz
	SRR17761268.fastq.gz	Fastqsanger.gz

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Circulating miR-499a-5p is a potential biomarker of MYH7-associated hypertrophic cardiomyopathy

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Base Editing Correction of a Hypertrophic Cardiomyopathy-Causing MYH7 Mutation in Human Cardiomyocytes and Humanized Mice

Project description:The most common form of genetic heart disease is hypertrophic cardiomyopathy (HCM), which is caused by mutations in cardiac sarcomeric genes and leads to abnormal heart muscle thickening. Complications of HCM include heart failure, arrhythmia, and sudden cardiac death. The dominant-negative c.1208 G>A (p.R403Q) mutation in b-myosin (MYH7) is a common and well-studied mutation that leads to increased cardiac contractility and HCM onset. Here we identify an adenine base editor (ABE) and single-guide RNA system that can efficiently correct this human pathogenic mutation with minimal off-target and bystander editing. We show that delivery of base editing components rescues pathological manifestations of HCM in iPSC-cardiomyocytes derived from HCM patients and in a humanized mouse model of HCM. Our findings demonstrate the use of base editing to treat inherited cardiac diseases and prompt the further development of ABE-based therapies to correct a variety of monogenic mutations causing cardiac disease.

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Project description:Base Editing Correction of a Hypertrophic Cardiomyopathy-Causing MYH7 Mutation in Human Cardiomyocytes and Humanized Mice

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Circulating miR-499a-5p Is a Potential Biomarker of <i>MYH7</i>-Associated Hypertrophic Cardiomyopathy.

Project description:Hypertrophic cardiomyopathy (HCM) is the most common inherited myocardial disease with significant genetic and phenotypic heterogeneity. To search for novel biomarkers, which could increase the accuracy of HCM diagnosis and improve understanding of its phenotype formation, we analyzed the levels of circulating miRNAs—stable non-coding RNAs involved in post-transcriptional gene regulation. Performed high throughput sequencing of miRNAs in plasma of HCM patients and controls pinpointed miR-499a-5p as one of 35 miRNAs dysregulated in HCM. Further investigation on enlarged groups of individuals showed that its level was higher in carriers of pathogenic/likely pathogenic (P/LP) variants in MYH7 gene compared to controls (fold change, FC = 8.9; p < 0.0001). Just as important, carriers of variants in MYH7 gene were defined with higher miRNA levels than carriers of variants in the MYBPC3 gene (FC = 14.1; p = 0.0003) and other patients (FC = 4.1; p = 0.0008). The receiver operating characteristic analysis analysis showed the ability of miR-499a-5p to identify MYH7 variant carriers with the HCM phenotype with area under the curve value of 0.95 (95% confidence interval: 0.88−1.03, p = 0.0004); sensitivity and specificity were 0.86 and 0.91 (cut-off = 0.0014). Therefore, miR-499a-5p could serve as a circulating biomarker of HCM, caused by P/LP variants in MYH7 gene.

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A novel miRNA screen identifies miRNA-4454 as a candidate biomarker for ventricular fibrosis in patients with hypertrophic cardiomyopathy

Project description:Left ventricular hypertrophy, myocardial disarray and interstitital fibrosis are the hallmarks of hypertrophic cardiomyopathy (HCM). Access to the myocardium for diagnostic purposes is limited. Circulating biomolecules reflecting the myocardial disease processes could improve early detection of HCM. Circulating miRNAs have been found to reflect disease processes in several cardiovascular diseases. Circulating miR-1, miR-495-3p and miR-4454 levels are elevated in plasma of HCM patients. miR-4454 is suggested as a potential biomarker for fibrosis in these patients.

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Project description:This study utilized TMT to characterize the cardiac proteomic differences between patients with hypertrophic cardiomyopathy and controls.

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