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Extracellular Vesicles From Liver Progenitor Cells Downregulates Fibroblast Metabolic Activity and Increase the Expression of Immune-Response Related Molecules

ABSTRACT: Extracellular Vesicles From Liver Progenitor Cells Downregulates Fibroblast Metabolic Activity and Increase the Expression of Immune-Response Related Molecules

PROVIDER: PRJNA659799 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12536515.fastq.gz	Fastqsanger.gz
	SRR12536516.fastq.gz	Fastqsanger.gz
	SRR12536517.fastq.gz	Fastqsanger.gz
	SRR12536518.fastq.gz	Fastqsanger.gz
	SRR12536519.fastq.gz	Fastqsanger.gz

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Extracellular Vesicles From Liver Progenitor Cells Downregulates Fibroblast Metabolic Activity and Increase the Expression of Immune-Response Related Molecules

Project description:Extracellular vesicles are an important part of cell to cell crosstalk, and help to the acceptor cells to prepare for changes in their environment. MLP29 cells are mouse liver progenitor cells that release EVs loaded with cell fate signaling. In the current work, we have fed 3T3-L1 mouse fibroblast with those EVs, and then analyzed the cellular response by proteomics and transcriptomics. Results showed a downregulation of both proteins and transcripts related to proliferative and metabolic routes dependent on TGFb, and an increase on the ERBB2 inhibitor protein (ERBIN). An increase in the transcription of CXCL2, as well as the increase of ribosome biogenesis and interferon response molecules points toward the activation of immune system signaling, compatible with a response against tissue damage.

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Extracellular Vesicles From Liver Progenitor Cells Downregulates Fibroblast Metabolic Activity and Increase the Expression of Immune-Response Related Molecules.

Project description:Extracellular vesicles (EVs) mediate cell-to-cell crosstalk whose content can induce changes in acceptor cells and their microenvironment. MLP29 cells are mouse liver progenitor cells that release EVs loaded with signaling cues that could affect cell fate. In the current work, we incubated 3T3-L1 mouse fibroblasts with MLP29-derived EVs, and then analyzed changes by proteomics and transcriptomics. Results showed a general downregulation of protein and transcript expression related to proliferative and metabolic routes dependent on TGF-beta. We also observed an increase in the ERBB2 interacting protein (ERBIN) and Cxcl2, together with an induction of ribosome biogenesis and interferon-related response molecules, suggesting the activation of immune system signaling.

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