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RNAseq of mitral valves from Fbn1 C1039G/+ mice with or without CCR2 deficiency

ABSTRACT: RNAseq of mitral valves from Fbn1 C1039G/+ mice with or without CCR2 deficiency

PROVIDER: PRJNA837252 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19170867_1.fastq.gz	Fastqsanger.gz
	SRR19170867_2.fastq.gz	Fastqsanger.gz
	SRR19170868_1.fastq.gz	Fastqsanger.gz
	SRR19170868_2.fastq.gz	Fastqsanger.gz
	SRR19170869_1.fastq.gz	Fastqsanger.gz

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RNAseq of mitral valves from Fbn1 C1039G/+ mice with or without CCR2 deficiency

Project description:Mitral valves were isolated from 2-month-old mice with the following 4 genotypes: 1) CCR2 RFP/+ (Chet), 2) CCR2 RFP/RFP (Cko), 3) Fbn1 C1039G/+; CCR2 RFP/+ (FhetChet), 4) Fbn1 C1039G/+; CCR2 RFP/RFP (FhetCko). N=4 for each genotype. Total RNA was extracted from mitral valves individually for gene expression profiling.

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Project description:Mitral and tricuspid valves are essential for unidirectional blood flow in the heart. They are derived from similar cell sources, and yet congenital dysplasia affecting both valves is clinically rare, suggesting the presence of differential regulatory mechanisms underlying their development. We specifically inactivated Dicer1 in the endocardium during cardiogenesis and found that Dicer1-deletion caused congenital mitral valve stenosis and regurgitation, while it had no impact on other valves. We showed that hyperplastic mitral valves were caused by abnormal condensation and extracellular matrix (ECM) remodeling. Our single-cell RNA Sequencing analysis revealed impaired maturation of mesenchymal cells and abnormal expression of ECM genes in mutant mitral valves. Furthermore, expression of a set of miRNAs that target ECM genes was significantly lower in tricuspid valves compared to mitral valves, consistent with the idea that the miRNAs are differentially required for mitral and tricuspid valve development. We thus reveal miRNA-mediated gene regulation as a novel molecular mechanism that differentially regulates mitral and tricuspid valve development, thereby enhancing our understanding of the non-association of inborn mitral and tricuspid dysplasia observed clinically.

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