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Redox-sensitive High-mobility group box-1 isoforms contribute to liver fibrosis progression and resolution in mice

ABSTRACT: To study role of different HMGB1 isoforms in liver fibrosis and resolution

ORGANISM(S): Mus musculus Rattus norvegicus

PROVIDER: GSE233751 | GEO | 2023/09/30

REPOSITORIES: GEO

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Redox-sensitive high-mobility group box-1 isoforms contribute to liver fibrosis progression and resolution in mice

Project description:Since oxidative stress plays a major role in liver fibrosis and induces post-translational modifications of proteins, we hypothesized that redox-sensitive HMGB1 isoforms contribute to liver fibrosis progression and resolution. This study is significant because a rise in [H] HMGB1 could flag 'patient at risk', the presence of [O] HMGB1 could suggest 'disease in progress or active scarring', while the appearance of [SO3] HMGB1 could point at 'resolution under way'. The latter could be used as a readout for response to pharmacological intervention with anti-fibrotic agents.

2024-02-21 | GSE240397 | GEO

Redox-sensitive High-mobility group box-1 isoforms contribute to liver fibrosis progression and resolution in mice

Project description:Redox-sensitive High-mobility group box-1 isoforms contribute to liver fibrosis progression and resolution in mice

| PRJNA977696 | ENA

Redox-sensitive high-mobility group box-1 isoforms contribute to liver fibrosis progression and resolution in mice

Project description:Redox-sensitive high-mobility group box-1 isoforms contribute to liver fibrosis progression and resolution in mice

| PRJNA1003497 | ENA

RNA sequencing of high mobility group box 1-treated melanocytes [hmgb1]

Project description:Purpose: Determine the mechanism of high mobility group box 1 (HMGB1)-induced signaling in melanocytes. Method: Primary human epidermal melanocytes were treated with HMGB1 (1 μg/ml) and incubated for 24 h. Total RNA (500 ng) from melanocytes were extracted and subjected to library synthesis. Results: HMGB1-treated melanocytes exhibited upregulation of cell death and type 1 interferon-related genes. Conclusion: HMGB1-induced melanocyte signaling was well evaluated using RNA sequencing.

2023-07-28 | GSE216423 | GEO

High Mobility Group Box Protein 1 is Dispensable for Autophagy and Mitochondrial Quality Control in Vivo

Project description:Gene expression of livers with hepatocyte-specific deletion of Hmgb1 was compared to control livers with floxed Hmgb1 Hmgb1-deleted livers (from mice expressing Albumin-Cre and floxed Hmgb1) and control liver (mice expressing only floxed Hmgb1) Whole liver from 8 week old mice was used. Both groups are littermates, and have been backcrossed to C57Bl/6 five times.

2016-04-11 | GSE49824 | GEO

Deficiency of neutrophil high-mobility group box-1 in liver transplant recipients exacerbates early allograft injury in mice

Project description:To investigate the role of recipient neutrophil intracellular HMGB1 in early allograft injury after liver transplant. Using a mouse orthotopic liver transplant model, as well as LPS injection, we found that neutrophils significantly infiltrate the liver after liver transplant and LPS challenge. Deficiency of neutrophil HMGB1 enhances their activation, boosts their pro-oxidant and pro-inflammatory phenotype, and hinders biosynthesis and metabolism of inositol polyphosphates. Overall, these events exacerbate early allograft injury after liver transplant.

2023-07-27 | GSE225106 | GEO

High-mobility group box1 peptide ameliorates bronchopulmonary dysplasia (BPD) via suppressing inflammation and fibrosis in a mouse model.

Project description:Previously, we have shown that a synthesized peptide originated from high mobility group box-1 protein (HMGB1) induces a regenerative cascade via activating endogenous mesenchymal stem cells in the body. Here, we have tested whether the HMGB1 peptide can ameliorate BPD related manifestations. In a mouse BPD model established by hyperoxia exposure, three shots of the HMGB1 peptide significantly improved the survival and lung function. Single-cell RNA-seq analysis on the lung showed that an inflammatory signature in macrophages and a fibrotic signature in fibroblasts induced by hyperoxia exposure were significantly suppressed by the HMGB1 peptide. These changes in transcriptome were also confirmed at the protein level. Together, the HMGB1 peptide treatment prevented the progression of BPD by suppressing inflammation and fibrosis. Our data serve as a foundation to develop new effective therapies for BPD.

2024-11-12 | GSE181497 | GEO

Identification of proteins interacting with cytoplasmic high-mobility group box 1 (HMGB1) during the hepatocellular response to ischemia reperfusion injury

Project description:Ischemia/reperfusion injury (IRI) occurs in liver transplantations and major resections and can lead to liver dysfunction. HMGB1 locates in nucleus of normal hepatocytes, but translocates to cytoplasm and the extracellular space during IRI. Although the functions of nuclear and extracellular HMGB1 are well explored, the role cytoplasmic HMGB1 plays in hepatic IRI is still unknown. We hypothesize cytoplasmic HMGB1 interacts with binding proteins involved in the hepatocellular response to IRI. In this study binding proteins of cytoplasmic HMGB1 during hepatic IRI were identified. Normal and warm ischemia reperfusion (WI/R) liver tissues were used for cytoplasmic protein extraction. The protein extracts were subjected to co-immunoprecipitation to enrich HMGB1-protein complexes. To identify the immunoprecipitated proteins in eluates, 2DE and subsequent MS detection were performed. Three identified proteins were verified using western blotting: betaine--homocysteine S-methyltransferase 1 (BHMT), cystathionine gamma-lyase (CTH) and ATP synthase beta subunit (ATP5B). All three identified proteins have a role in metabolic pathways and autophagy. Our results demonstrate cytoplasmic HMGB1 binds to BHMT, CTH and ATP5B during hepatic WI/R. Since both, cytoplasmic HMGB1 and binding proteins, are involved in autophagy, we speculate this protein complex may be involved in the hepatocellular response to IRI via the autophagy pathway.

2017-03-10 | PXD003538 | Pride

Characterization of an Entamoeba histolytica High-Mobility-Group Box Protein Induced during Intestinal Infection

Project description:The unicellular eukaryote Entamoeba histolytica is a human parasite that causes amebic dysentery and liver abscess. A genome-wide analysis of gene expression modulated by intestinal colonization and invasion identified an up-regulated transcript that encoded a putative high-mobility-group box (HMGB) protein, EhHMGB1. We tested if EhHMGB1 encoded a functional HMGB protein, and determined its role in control of parasite gene expression. Recombinant EhHMGB1 was able to bend DNA in vitro, a characteristic of HMGB proteins. Core conserved residues required for DNA bending activity in other HMGB proteins were demonstrated by mutational analysis to be essential for EhHMGB1 activity. EhHMGB1 was also able to enhance the binding of human p53 to its cognate DNA sequence in vitro, which is expected for an HMGB1 protein. Confocal microscopy, using antibodies against the recombinant protein, confirmed its nuclear localization. Overexpression of EhHMGB1 in HM1: IMSS trophozoites led to modulation of 33 transcripts involved in a variety of cellular functions. Of these, twenty were also modulated at either day one or day 29 in the mouse model of intestinal amebiasis. Notably, four transcripts with known roles in virulence, including two encoding Gal/GalNAc lectin light chains, were modulated in response to EhHMGB1 overexpression. We concluded that EhHMGB1 was a bona fide HMGB protein with the capacity to recapitulate part of the modulation of parasite gene expression seen during adaptation to the host intestine. 6 samples for two groups: 3M and Gir. Each groups contain 3 samples

2008-11-19 | E-GEOD-12204 | biostudies-arrayexpress

Investigating the effects of different HMGB1 redox isoforms on macrophage polarization

Project description:Macrophages are key inflammatory immune cells that display dynamic phenotypes and functions in response to their local microenvironment. In different conditions, macrophage polarization can be induced by high-mobility group box 1 (HMGB1), a nuclear DNA-binding protein that activates innate immunity. This study investigated the phenotypes of murine bone-marrow-derived macrophages (BMDMs) induced by different HMGB1 redox isoforms via bulk RNA sequencing (RNAseq).

2022-06-02 | GSE200210 | GEO

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