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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE49824 | GEO | 2016/04/11

SECONDARY ACCESSION(S): PRJNA215026

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.

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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

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

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

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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

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

Gene expression profiling of HDAC3-depleted mouse liver rescued with wild-type exogenous HDAC3

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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

Chromatin IP sequencing of the nuclear factor HMGB1 in livers from mice after a metabolic stress either induced by a 12-week high fat diet consumption or a fasting (6hours)-refeeding (8hours) challenge.

Project description:To unveil HMGB1 DNA occupancy in livers of mice after a metabolic stress either induced by a 12-week high fat diet consumption or a fasting (6hours)-refeeding (8hours) challenge. Challenges known to generate a robust activation of hepatic lipogenesis and liver steatosis.

2022-03-31 | E-MTAB-11543 | biostudies-arrayexpress

Gene expression profiling of HDAC3-depleted mouse liver rescued with wild-type exogenous HDAC3

Project description:We have shown that intravenous injection of HDAC3 floxed mice with adeno-associated virus (AAV) expressing Cre depletes hepatic HDAC3, upregulates lipogenic gene expression, and causes fatty liver. When AAV-Flag-HDAC3 wild-type (WT) is co-injected along with AAV-Cre, the exogenous HDAC3 is expressed at endogenous levels and can completely rescue fatty liver phenotype. Here we profile transcriptome of the rescued WT livers in comparison with HDAC3-depleted (KO) livers. 4-months old C57BL/6 male mice were co-injected with AAV-Cre or AAV-Cre plus AAV-Flag-HDAC3. Mice were fed ad libitum and harvested at 5 pm (ZT10) at 2-weeks post-injection. Liver total RNA was extracted and hybridized to Affymetrix Mouse Gene 1.0ST array.

2013-11-25 | E-GEOD-49386 | biostudies-arrayexpress

LKB1 and Notch deletion in mouse liver

Project description:We characterize the phenotype of mice in which the deletion of Lkb1 has been targeted in the liver. Lack of Lkb1 in the liver results in bile duct paucity leading to cholestasis. This phenotype is similar to that obtained upon inactivation of Notch signaling in the liver. We test the hypothesis of a functional overlap between the Lkb1 and Notch pathways by gene expression profiling of livers deficent in Lkb1 or in the Notch mediator RbpJκ. We used AlfpCre mice for liver-specific deletion of LKB1 that were crossed with a conditional knockout mouse model (LKB1 floxed mice). We used also AlfpCre mice for liver-specific inactivation of the Notch pathway. AlfpCre mice were crossed with the RbpJκ floxed mice. RNA was extracted from the liver of LKB1 KO mice (Lkb1Floxed, AlfpCre positive mice) and their wild-type counterpart (Lkb1Floxed, AlfpCre negative mice). RNA was also extracted from liver of RbpJK KO mice (RbpJK floxed, AlfpCre positive) and their wild type mice (RbpJK floxed, AlfpCe negative).

2015-12-08 | GSE75564 | GEO

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