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Osr1-mediated mesothelial transition of liver mesenchymal cells exacerbates fibrotic liver damage

ABSTRACT: Osr1-mediated mesothelial transition of liver mesenchymal cells exacerbates fibrotic liver damage

PROVIDER: PRJNA1063625 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27497783_1.fastq.gz	Fastqsanger.gz
	SRR27497783_2.fastq.gz	Fastqsanger.gz
	SRR27497784_1.fastq.gz	Fastqsanger.gz
	SRR27497784_2.fastq.gz	Fastqsanger.gz
	SRR27497785_1.fastq.gz	Fastqsanger.gz

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Osr1-mediated mesothelial transition of liver mesenchymal cells exacerbates fibrotic liver damage

Project description:In chronic liver diseases, hepatic stellate cells (HSCs) are induced to form the myofibroblasts responsible for scar formation, leading to liver fibrosis and cirrhosis. Here, single-cell RNA sequencing with in vivo lineage tracing in non-alcoholic steatohepatitis (NASH) model mice reveals a subpopulation of HSCs transitioning back to a state resembling their developmental precursors, mesothelial cells (MCs), after liver injury. These damage-associated intermediates between HSCs and MCs (DIHMs) can be traced with a dual recombinase system by labeling Krt19-expressing cells within pre-labeled Pdgfrb-positive HSCs, and DIHMs highly express inflammation- and fibrosis-associated genes. Cre and Dre-inducible depletion of DIHMs by administering diphtheria toxin reduces liver fibrosis and alleviates liver damage in NASH model mice. Importantly, knockdown of Osr1, a zinc finger transcription factor of the OSR gene family, can block DIHM induction in vitro. Conditional knockout Osr1 in Pdgfrb-expressing mesenchymal cells in NASH model mice can reduce liver fibrosis in vivo. Our study collectively uncovers an injury-induced developmental reversion process wherein HSCs undergo what we term a mesenchymal-to-mesothelial transition (MMesoT), which can be targeted to develop interventions to treat chronic liver diseases.

2024-01-12 | GSE252999 | GEO

Expression data from fetal and adult mouse liver mesothelial cells

Project description:Characterization and Functional Analyses of Hepatic Mesothelial Cells in Mouse Liver Development. We used microarrays to detail the global programme of gene expression in mesothelial cells during mouse liver development. Mouse liver mesothelial cells were selected by a cell sorter at E12.5 and adult for RNA extraction and hybridization on Affymetrix microarrays. We obtained PCLP1+ cells and Mesothelin+ cells at each developmental stage in order to analyze expression profiles of mesothelial cells.

2009-11-09 | E-GEOD-18937 | biostudies-arrayexpress

Clusterin is protective for liver fibrosis through mesothelial-specific LRP2 receptor mediated endocytosis

Project description:During liver fibosis, the CLU protein was overexpressed of hepatocytes. Loss of function perform showed that CLU is protective for liver fibrosis. Mechanismly, we found LRP2 postive cells were increased after hrCLU administration in fibrotic CLUKO mice. Then single cell analysis domenstrated that LRP2 positive cells were mesothelial cells, which play a critical role of endocytosis during fibrosis resolution. Taken together, we identify clusterin as a protective chaperone that can reverse liver fibrosis and clear extracellular matrix, which targets LRP2 signaling mediated endocytosis.

2024-06-01 | GSE235221 | GEO

Expression data from fetal and adult mouse liver mesothelial cells

2009-11-10 | GSE18937 | GEO

iTRAQ proteomics of non fibrotic carcinoma on Human Liver

Project description:We present a study of hepatocellular carcinoma developed on non-fibrotic liver (nfHCC) that combines complementary quantitative iTRAQ-based proteomics and phosphoproteomics approaches. Using both approaches, we analyzed a set of 24 samples (18 nfHCC vs 6 non-tumor liver tissue).

2014-09-18 | PXD001253 | Pride

Expression of genes in E17 p57-/- and p57+/+ hepatic mesothelial and submesothelial cells

Project description:To analyze p57 function in mouse fetal liver, we surgically isolated mesothelial and submesothelial cells from E17 p57-/- and p57+/+ livers. Compared gene expression in E17 p57-/- and p57+/+ hepatic mesothelial and submesothelial cells.

2014-10-01 | E-GEOD-61010 | biostudies-arrayexpress

Bulk RNA-seq of fibroblasts and mesothelial cells from healthy mouse tissues

Project description:Bulk RNA-seq was performed on fibroblasts and mesothelial cells from 11 different healthy mouse tissues such as bone, epididymal, brown and inguinal fat pads, mesentery, omentum, pancreas, liver, lung, lymph node and spleen. This data was used to examine tissue specific gene expression programs of fibroblasts and mesothelial cells.

2021-05-04 | E-MTAB-10324 | biostudies-arrayexpress

Expression profiling of prognostic liver signature in clinical fibrotic liver tissues cultured with various anti-fibrotic and chemopreventive agents

Project description:Expression profiling of prognostic liver signature in clinical fibrotic liver tissues cultured with various anti-fibrotic and chemopreventive agents

| PRJNA754395 | ENA

Expression profiling of prognostic liver signature in clinical fibrotic liver tissues cultured with various anti-fibrotic and chemopreventive agents

Project description:Background/Aims: There is a major unmet need to assess prognostic impact of anti-fibrotics in clinical trials due to the slow rate of liver fibrosis progression. We aimed to develop a surrogate biomarker to predict future fibrosis progression. Methods: A Fibrosis Progression Signature (FPS) was defined to predict fibrosis progression within 5 years in HCV and NAFLD patients with no to minimal fibrosis at baseline (n=421), and validated in an independent NAFLD cohort (n=78). The FPS was used to assess response to 13 candidate anti-fibrotics in organotypic ex vivo cultures of clinical fibrotic liver tissues (n=78), and cenicriviroc in NASH patients enrolled in a clinical trial (n=19, NCT02217475). A serum-protein-based surrogate FPS (FPSec) was developed and technically evaluated in a liver disease patient cohort (n=79). Results: A 20-gene FPS was defined and validated in an independent NAFLD cohort (aOR=10.93, AUROC=0.86). Among computationally inferred fibrosis-driving FPS genes, BCL2 was confirmed as a potential pharmacological target using clinical liver tissues. Systematic ex vivo evaluation of 13 candidate anti-fibrotics identified rational combination therapies based on epigallocatechin gallate, some of which were validated for enhanced anti-fibrotic effect in ex vivo culture of clinical liver tissues. In NASH patients treated with cenicriviroc, FPS modulation was associated with 1-year fibrosis improvement accompanied by suppression of the E2F pathway. Induction of PPAR-alfa pathway was absent in patients without fibrosis improvement, suggesting benefit of combining PPAR-alfa agonism to improve anti-fibrotic efficacy of cenicriviroc. A 7-protein FPSec panel showed concordant prognostic prediction with FPS. Conclusion: FPS predicts long-term fibrosis progression in an etiology-agnostic manner, which can inform anti-fibrotic drug development.

2021-12-22 | GSE182065 | GEO

Expression profiling of Prognostic Liver Signature and fibrosis-related genes in clinical fibrotic liver tissue cultured with various anti-fibrotic agents

Project description:Background/Aims: There is a major unmet need to assess prognostic impact of anti-fibrotics in clinical trials due to the slow rate of liver fibrosis progression. We aimed to develop a surrogate biomarker to predict future fibrosis progression. Methods: A Fibrosis Progression Signature (FPS) was defined to predict fibrosis progression within 5 years in HCV and NAFLD patients with no to minimal fibrosis at baseline (n=421), and validated in an independent NAFLD cohort (n=78). The FPS was used to assess response to 13 candidate anti-fibrotics in organotypic ex vivo cultures of clinical fibrotic liver tissues (n=78), and cenicriviroc in NASH patients enrolled in a clinical trial (n=19, NCT02217475). A serum-protein-based surrogate FPS (FPSec) was developed and technically evaluated in a liver disease patient cohort (n=79). Results: A 20-gene FPS was defined and validated in an independent NAFLD cohort (aOR=10.93, AUROC=0.86). Among computationally inferred fibrosis-driving FPS genes, BCL2 was confirmed as a potential pharmacological target using clinical liver tissues. Systematic ex vivo evaluation of 13 candidate anti-fibrotics identified rational combination therapies based on epigallocatechin gallate, some of which were validated for enhanced anti-fibrotic effect in ex vivo culture of clinical liver tissues. In NASH patients treated with cenicriviroc, FPS modulation was associated with 1-year fibrosis improvement accompanied by suppression of the E2F pathway. Induction of PPARalpha pathway was absent in patients without fibrosis improvement, suggesting benefit of combining PPARalpha agonism to improve anti-fibrotic efficacy of cenicriviroc. A 7-protein FPSec panel showed concordant prognostic prediction with FPS. Conclusion: FPS predicts long-term fibrosis progression in an etiology-agnostic manner, which can inform anti-fibrotic drug development.

2021-12-22 | GSE181538 | GEO

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