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

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

PROVIDER: PRJNA933103 | ENA |

REPOSITORIES: ENA

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Acetate controls endothelial-to-mesenchymal transition during atherosclerosis

Project description:Acetate controls endothelial-to-mesenchymal transition during atherosclerosis

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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

Project description:This SuperSeries is composed of the SubSeries listed below.

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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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BW25113 glucose to acetate transition

Project description:In bacterial adaptation to the dynamic environment, metabolic genes are typically thought to be the executors, whereas global transcription regulators are regarded as the decision makers. Although the feedback from metabolic consequence is believed to be important, much less is understood. This work demonstrates that the gluconeogenic genes in Escherichia coli, ppsA, sfcA, and maeB, provide a feedback loop to the global regulator, CRP, in carbon source transition. Disruption of one of the gluconeogenic pathways has no phenotype in balanced growth, but causes a significant delay in the diauxic transition from glucose to acetate. To investigate the underlying mechanism, we measured the transcriptome profiles during the transition using DNA microarray, and Network Component Analysis was employed to obtain the transcription factor activities. Results showed that one of the global regulators, CRP, was insufficiently activated during the transition in the ppsA deletion mutant. Indeed, addition of cAMP partially rescued the delay in transition. These results suggest that the gluconeogenic flux to phosphoenolpyruvate is important for full activation of adenylate cyclase through phosphorylated enzyme IIAglu of the phosphotransferase system. Reduction of this flux causes insufficient activation of CRP and a global metabolic deficiency, which exemplifies a significant feedback interaction from metabolism to the global regulatory system. Keywords: Time course Cells were grown up in M9 glucose media until mid log phase, then harvested and transitioned into M9 acetate media. Samples were taken immediately prior to transition to acetate (reference sample) and at 5, 15, 30, 60, 120, 180, 240, 300, and 360 minutes after transition.

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