RNAseq of mitral valves from Fbn1 mutant and control mice at 5 months
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE137681 | GEO | 2020/02/27
REPOSITORIES: GEO
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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:RNAseq of mitral valves from Fbn1 mutant and control mice at 5 months
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Project description:Whole mitral valves from each Whitney grade of disease; normal (n=6), grade 1 (n=5), grade 2 (n=6), grade 3 (n=6) and grade 4 (n=5). mRNA was extracted using the qiagen RNeasy minikit and assessed by the agilent 2200 bioanalsyser. all samples passed quality control and transcriptomic analysis was performed by edinburgh genomics using the Affymetrix GeneChip™ Canine Gene 1.1ST Array. Results were reported as CEL files and then analysed in Affymetrix expression console (version 1.4.1.46) using the canine 1.1ST library files from Affymetrix. Robust Multi-array Average (RMA) was used to perform gene level normalisation and signal level summarisation.Following this, quality control assessment was performed on the data set. This included assessment of hybridisation (spike in) controls, labelling (poly-A) controls and area under the curve (AUC) control, probe cell intensity boxplots, a signal histogram graph and principle component analysis (PCA) plot. Following this assessment, the datasets were exported with annotation as a text file or as a CHT file. Affymetrix transcriptome analysis console (version 3.1.0.5) was used to perform unpaired one-way analysis of variance (ANOVA).
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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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