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Acetate controls endothelial-to-mesenchymal transition during atherosclerosis

ABSTRACT: Acetate controls endothelial-to-mesenchymal transition during atherosclerosis

PROVIDER: PRJNA933152 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23381561_1.fastq.gz	Fastqsanger.gz
	SRR23381561_2.fastq.gz	Fastqsanger.gz
	SRR23381562_1.fastq.gz	Fastqsanger.gz
	SRR23381562_2.fastq.gz	Fastqsanger.gz
	SRR23381563_1.fastq.gz	Fastqsanger.gz

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Acetate controls endothelial-to-mesenchymal transition during atherosclerosis [1]

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Acetate controls endothelial-to-mesenchymal transition during atherosclerosis [2]

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Acetate controls endothelial-to-mesenchymal transition during atherosclerosis

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Acetate controls endothelial-to-mesenchymal transition.

Project description:Endothelial-to-mesenchymal transition (EndMT), a process initiated by activation of endothelial TGF-β signaling, underlies numerous chronic vascular diseases and fibrotic states. Once induced, EndMT leads to a further increase in TGF-β signaling, thus establishing a positive-feedback loop with EndMT leading to more EndMT. Although EndMT is understood at the cellular level, the molecular basis of TGF-β-driven EndMT induction and persistence remains largely unknown. Here, we show that metabolic modulation of the endothelium, triggered by atypical production of acetate from glucose, underlies TGF-β-driven EndMT. Induction of EndMT suppresses the expression of the enzyme PDK4, which leads to an increase in ACSS2-dependent Ac-CoA synthesis from pyruvate-derived acetate. This increased Ac-CoA production results in acetylation of the TGF-β receptor ALK5 and SMADs 2 and 4 leading to activation and long-term stabilization of TGF-β signaling. Our results establish the metabolic basis of EndMT persistence and unveil novel targets, such as ACSS2, for the potential treatment of chronic vascular diseases.

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Project description:To investigate the transcriptome of endothelial cells undergoing endothelial-to-mesenchymal transition, transcription profiling was performed on primary human endothelial cells in the presence or absence of 40mM acetate following control or cytokine treatment for 4 days. We then performed gene expression profiling analysis using data obtained from RNA-seq of primary human endothelial cells.

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Multiomic profiling of in vitro models of endothelial-to-mesenchymal transition reveals endothelial cell subtype is a major determinant of fidelity to observed states in atherosclerosis

Project description:Endothelial-to-mesenchymal transition (EndMT) is an example of endothelial cell (EC) heterogeneity which is commonly modeled in vitro to better understand driving mechanisms of disease proceses, including atherosclerosis. We used multi-modal single nucleus RNA sequencing (snRNA-seq) and ATAC sequencing (snATAC-seq) to analyze the diversity of ECs in vitro, divergent EC responses to known EndMT perturbations, and the ability of in vitro EC known EndMT models to recapitulate the in vivo 'omic profiles of cells observed in atherosclerosis.

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