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Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (mRNA-Seq)

ABSTRACT: To elucidate the molecular mechanisms underlying the roles of inflammatory cells in scar formation, we performed RNA-seq of inflammation-related mRNAs and miRNAs from both wild-type mice and PU.1 knock-out mice (PU.1 KO). This approach allowed us to comprehensively investigate how inflammation-related gene expression influences the skin wound healing process.

ORGANISM(S): Mus musculus

PROVIDER: GSE234270 | GEO | 2024/09/30

REPOSITORIES: GEO

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Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (Spatial Gene Expression)

Project description:Spatial transcriptome analysis (Visium, 10x Genomics) was performed to define the spatial topography of inflammation-related gene expressions in microenvironments of wound tissues.

2024-09-30 | GSE234271 | GEO

Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling.

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

2024-09-30 | GSE234272 | GEO

Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (single cell RNA-Seq)

Project description:To understand the molecular mechanism of minority cell population in skin would healing process, we performed single cell RNA sequencing (scRNA-seq) of murine skin wound tissues at 3 different time points after injury (3d, 7d, 14d).

2024-09-30 | GSE234269 | GEO

Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling.

Project description:Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling.

| PRJNA980665 | ENA

Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (mRNA-Seq)

Project description:Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (mRNA-Seq)

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Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (Spatial Gene Expression)

Project description:Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (Spatial Gene Expression)

| PRJNA980674 | ENA

Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (single cell RNA-Seq)

Project description:Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (single cell RNA-Seq)

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Hypochlorite-induced porcine model of peritoneal fibrosis through the activation of IL1β-CX3CL1-TGFβ1 signal axis.

Project description:Patients with kidney failure rely on life-saving peritoneal dialysis to facilitate waste exchange and maintain homeostasis of physical conditions. However, peritoneal dialysis often results in peritoneal fibrosis and organ adhesion that subsequently compromise the efficiency of peritoneal dialysis and normal functions of visceral organs. Despite rodent models provide clues on the pathogenesis of peritoneal fibrosis, no current large animal model which shares high degree of physiological and anatomical similarities to human is available, limiting their applications on the evaluation of pre-clinical therapeutic efficacy. Here we established for the first time, hypochlorite-induced porcine model of peritoneal fibrosis in 5-week-old piglets. We showed that administration 15-30 mM hypochlorite, a dose- and time-dependent severity of peritoneal fibrosis characterized by mesothelium fragmentation, αSMA+ myofibroblasts accumulation, organ surface thickening and type I collagen deposition were observed. We also demonstrated in vitro using human mesothelial cells that hypochlorite-induced fibrosis was likely due to necrosis, but not programmed apoptosis; besides, overexpression of IL1β, CX3CL1 and TGFβ on the peritoneal mesothelium in current model was detected, similar to observations from peritoneal dialysis-induced peritoneal fibrosis in human patients and earlier reported mouse model. Moreover, our novel antemortem evaluation using laparoscopy provided instant feedback on the progression of organ fibrosis/adhesion which allows immediate adjustments on treatment protocols and strategies in alive individuals that can not and never be performed in other animal models.

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Characterization of gene expression profiles in HBV-related liver fibrosis patients and identification of ITGBL1 as a key regulator of fibrogenesis.

Project description:Although hepatitis B virus (HBV) infection is the leading cause of liver fibrosis (LF), the mechanisms underlying liver fibrotic progression remain unclear. Here, we investigated the gene expression profiles of HBV-related LF patients. Whole genome expression arrays were used to detect gene expression in liver biopsy samples from chronically HBV infected patients. Through integrative data analysis, we identified several pathways and key genes involved in the initiation and exacerbation of liver fibrosis. Weight gene co-expression analysis revealed that integrin subunit β-like 1 (ITGBL1) was a key regulator of fibrogenesis. Functional experiments demonstrated that ITGBL1 was an upstream regulator of LF via interactions with transforming growth factor β1. In summary, we investigated the gene expression profiles of HBV-related LF patients and identified a key regulator ITGBL1. Our findings provide a foundation for future studies of gene functions and promote the development of novel antifibrotic therapies.

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Inactivation of Sox9 in fibroblasts reduces cardiac fibrosis and inflammation in mice after myocardial infarction

Project description:Fibrotic scarring drives the progression of heart failure after myocardial infarction (MI). Therefore, the development of specific treatment regimens to counteract fibrosis is of high clinical relevance. The transcription factor SOX9 functions as an important regulator during embryogenesis, but recent data point towards an additional causal role in organ fibrosis. We show here that SOX9 is upregulated in the scar after MI in mice. Fibroblast specific deletion of Sox9 ameliorated MI-induced left ventricular dysfunction, dilatation and myocardial scarring in vivo. Unexpectedly, deletion of Sox9 also potently eliminated persisting leukocyte infiltration of the scar in the chronic phase after MI. RNA-sequencing from the infarct scar revealed that Sox9 deletion in fibroblasts resulted in strongly downregulated expression of genes related to extracellular matrix, proteolysis and inflammation. Importantly, Sox9 deletion in isolated cardiac fibroblasts in vitro similarly affected gene expression as in the cardiac scar and prevented their activation and myofibroblast differentiation. Together, our data demonstrate that fibroblast SOX9 functions as a master regulator of cardiac fibrosis and inflammation and might constitute a novel therapeutic target during MI.

2019-07-25 | GSE132265 | GEO

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