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Portal fibroblasts with mesenchymal stem cell features form a reservoir of proliferative myofibroblasts in liver fibrosis

ABSTRACT: Portal fibroblasts with mesenchymal stem cell features form a reservoir of proliferative myofibroblasts in liver fibrosis

PROVIDER: PRJNA688690 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13329200_1.fastq.gz	Fastqsanger.gz
	SRR13329200_2.fastq.gz	Fastqsanger.gz
	SRR13329201_1.fastq.gz	Fastqsanger.gz
	SRR13329201_2.fastq.gz	Fastqsanger.gz
	SRR13329202_1.fastq.gz	Fastqsanger.gz

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Portal fibroblasts with mesenchymal stem cell features form a reservoir of proliferative myofibroblasts in liver fibrosis

Project description:Portal fibroblasts with mesenchymal stem cell features form a reservoir of proliferative myofibroblasts in liver fibrosis

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Portal fibroblasts with mesenchymal stem cell features form a reservoir of proliferative myofibroblasts in liver fibrosis

Project description:Portal fibroblasts with mesenchymal stem cell features form a reservoir of proliferative myofibroblasts in liver fibrosis

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Portal fibroblasts with mesenchymal stem cell features form a reservoir of proliferative myofibroblasts in liver fibrosis

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Portal fibroblasts with mesenchymal stem cell features form a reservoir of proliferative myofibroblasts in liver fibrosis

Project description:Portal mesenchymal cells represent a very small amount of cells. They are tightly bound to the bile duct and portal vascular structures, relying on basement membranes. In the present study, we set up a specific procedure to isolate portal mesenchymal cells, for scRNAseq analysis. We identified 16 distinct cell clusters, including fibroblasts (5 clusters), vascular smooth muscle cells (VSCMs, 5 clusters), endothelial cells (4 clusters), HSCs (1 cluster) and mesothelial cells (1 cluster).

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Portal fibroblasts with mesenchymal stem cell features form a reservoir of proliferative myofibroblasts in liver fibrosis

Project description:We performed transcriptomic studies comparing phenotypically defined PMSCs (PDGFRa/CD34/CD9high:CD200low) to HSCs (Vitamin-A fluorescent) of high purity, using bulk RNAseq. We further extended bulk RNAseq analyses of the two cell populations to myofibroblasts derived from both cell types in culture, including an early and late stage of differentiation for PMSC-MFs. Comparative analyses of gene expression indicated that 100 genes in PMSCs and 112 genes in HSCs, i) were overexpressed according to both scRNAseq and bulk RNAseq analyses, and ii) remained differentially expressed in these cells throughout their myofibroblastic differentiation. We selected the most differentially expressed of these genes, to build a multigene expression signature of PMSCs/PMSC-MFs (7 genes) and of HSCs/HSC-MFs (6 genes).

2021-03-31 | GSE164037 | GEO

Portal fibroblasts with mesenchymal stem cell features form a reservoir of proliferative myofibroblasts in liver fibrosis

Project description:Based on the identification of a transcriptomic signature, including Slit2, characterizing portal mesenchymal stem cells (PMSC) and derived myofibroblast (MF), we examined the gene expression profile of in liver tissue derived from multiple human liver disorders, including primary sclerosing cholangitis (PSC) (n=12), non-alcoholic steatohepatitis (NASH) (n=7) and other liver diseases (i.e., primary biliary cholangitis, autoimmune hepatitis, alcoholic liver disease and haemochromatosis) (n=8) and compared them to healthy controls (tumor free tissue from livers with metastasis from colorectal cancer) (n=5). We found that SLIT2 was overexpressed in the liver of patients with NASH, PSC and other chronic liver diseases. We also examined the microarray data of the human liver tissue samples for the transcriptomic signatures and found that in the different types of liver diseases the gene signature of PMSCs/PMSC-MFs was increased compared to normal liver, and correlated with the expression of ACTA2, COL1A1 and vWF.

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Portal fibroblasts with mesenchymal stem cell features form a reservoir of proliferative myofibroblasts in liver fibrosis

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

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Cancer-derived myofibroblasts vs. non-cancer derived myofibroblasts

Project description:All samples are conditioned media from primary cultured human gastric myofibroblasts, derived from either carcinoma tissue, or adjacent non cancerous tissue. In each experiment the cancer-derived myofibroblasts are compared against the non-cancer derived myofibroblasts from the same patient. All of the experiments were samples from Patient 1, except for 648, which is from Patient 2. SILAC labelling in each case is; 567 - Methionine COFRADIC; Cancer-derived = Heavy, Non-cancer = Light 575 - N-terminal COFRADIC; Cancer-derived = Heavy, Non-cancer = Light 646 - Cancer-derived = Light, Non-cancer = Heavy 647 - Non-cancer = Heavy, Non-cancer = Light (same cell line labelled twice to create a control experiment) 648 - Cancer-derived = Heavy, Non-cancer = Light

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Project description:Renal fibrosis is a common pathological endpoint that is challenging to reverse in chronic kidney disease (CKD) independently of the underlying causes. Although myofibroblasts are mainly responsible for the accumulation of a fibrillar collagen-rich extracellular matrix (ECM), recent reports revealed their heterogeneity in proliferative and fibrotic activities, mirroring specific metabolic states that drive fibrosis. Here, we investigate the role of E3 ubiquitin-protein ligase WWP2 in the metabolic reprogramming of renal myofibroblasts in fibrosis. The tubulointerstitial expression of WWP2 contributes to the progression of fibrosis in CKD patients and in pre-clinical models of CKD. WWP2 deficiency leads to increased fatty acid oxidation, boosting mitochondrial respiration, promoting myofibroblast proliferation and arresting pro-fibrotic activation, thus ameliorating kidney fibrosis. Specifically, WWP2 suppresses the transcription of PGC-1α, which mediates the metabolic and proliferative changes in fibrotic myofibroblasts. Pharmacological intervention targeting PGC-1α reverses the pro-fibrotic effect of WWP2. These findings reveal a previously unappreciated WWP2-PGC-1α axis underlying the metabolic reprogramming of myofibroblasts during renal fibrosis, which could provide a new target for therapeutic intervention in CKD.

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