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Cellular composition of murine mitral valves during autoimmune valvular carditis

ABSTRACT: Cellular composition of murine mitral valves during autoimmune valvular carditis

PROVIDER: PRJNA913174 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22793100.fastq.gz	Fastqsanger.gz
	SRR22793101.fastq.gz	Fastqsanger.gz
	SRR22793102.fastq.gz	Fastqsanger.gz
	SRR22793103.fastq.gz	Fastqsanger.gz
	SRR22793104.fastq.gz	Fastqsanger.gz

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Cellular composition of murine mitral valves during autoimmune valvular carditis

Project description:To characterize the cell types that compose the mitral valve during the development of autoimmune valvular carditis, we utilized scRNA sequencing. Live cells from inflamed valves of K/B.g7 mice or uninflamed B.g7 controls were collected and analyzed at 3-, 8-, and 25 weeks of age.

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

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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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Project description:Congenital heart malformations include mitral valve defects, which remain largely unexplained. During embryogenesis, a restricted population of endocardial cells within the atrioventricular canal undergoes an endothelial-to-mesenchymal transition to give rise to mitral valvular cells. However, the identity and fate decisions of these progenitors as well as the behavior and distribution of their derivatives in valve leaflets remain unknown. We used single-cell RNA sequencing (scRNA-seq) of genetically labeled endocardial cells and microdissected mouse embryonic and postnatal mitral valves to characterize the developmental road. We defined the metabolic processes underlying the specification of the progenitors and their contributions to subtypes of valvular cells. Using retrospective multicolor clonal analysis, we describe specific modes of growth and behavior of endocardial cell-derived clones, which build up, in a proper manner, functional valve leaflets. Our data identify how both genetic and metabolic mechanisms specifically drive the fate of a subset of endocardial cells toward their distinct clonal contribution to the formation of the valve.

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Affymetrix GeneChip™ Canine Gene 1.1ST Array of canine heart valves in all stages of Myxomatous mitral valve disease (Normal-4)

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2019-12-26 | E-MTAB-8618 | biostudies-arrayexpress

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