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Further inhibition of Histone H2A ubiquitination protects myocardium against ischemia/reperfusion injury through enhancing glycolysis and improving mitochondrial function via promoting Hsp27 expression [I]

ABSTRACT: RNA-seq was undertaken in rats with or without myocardial ischemia-reperfusion injury to derive a list of signaling pathways and differentially expressed genes

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE225245 | GEO | 2023/12/27

REPOSITORIES: GEO

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Further inhibition of Histone H2A ubiquitination protects myocardium against ischemia/reperfusion injury through enhancing glycolysis and improving mitochondrial function via promoting Hsp27 expression [III]

Project description:H2Aub Chip-seq was undertaken in rats with myocardial ischemia injury to derive a list of signaling pathways and genes

2023-12-27 | GSE225538 | GEO

Project description:RNA-seq was undertaken in rats with or without myocardial ischemia injury to derive a list of signaling pathways and differentially expressed genes

2023-12-27 | GSE225368 | GEO

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

2023-12-27 | GSE225371 | GEO

Project description:Further inhibition of Histone H2A ubiquitination protects myocardium against ischemia/reperfusion injury through enhancing glycolysis and improving mitochondrial function via promoting Hsp27 expression

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Enhancing Glycolysis Protects against Ischemia-Reperfusion Injury by Reducing ROS Production.

Project description:After myocardial ischemia-reperfusion, fatty acid oxidation shows fast recovery while glucose oxidation rates remain depressed. A metabolic shift aimed at increasing glucose oxidation has shown to be beneficial in models of myocardial ischemia-reperfusion. However, strategies aimed at increasing glucose consumption in the clinic have provided mixed results and have not yet reached routine clinical practice. A better understanding of the mechanisms underlying the protection afforded by increased glucose oxidation may facilitate the transfer to the clinic. The purpose of this study was to evaluate if the modulation of reactive oxygen species (ROS) was involved in the protection afforded by increased glucose oxidation. Firstly, we characterized an H9C2 cellular model in which the use of glucose or galactose as substrates can modulate glycolysis and oxidative phosphorylation pathways. In this model, there were no differences in morphology, cell number, or ATP and PCr levels. However, galactose-grown cells consumed more oxygen and had an increased Krebs cycle turnover, while cells grown in glucose had increased aerobic glycolysis rate as demonstrated by higher lactate and alanine production. Increased aerobic glycolysis was associated with reduced ROS levels and protected the cells against simulated ischemia-reperfusion injury. Furthermore, ROS scavenger N-acetyl cysteine (NAC) was able to reduce the amount of ROS and to prevent cell death. Lastly, cells grown in galactose showed higher activation of mTOR/Akt signaling pathways. In conclusion, our results provide evidence indicating that metabolic shift towards increased glycolysis reduces mitochondrial ROS production and prevents cell death during ischemia-reperfusion injury.

| S-EPMC7240969 | biostudies-literature

Histone H2A variants alpha1-extension helix directs RNF168-mediated ubiquitination.

Project description:Histone ubiquitination plays an important role in the DNA damage response (DDR) pathway. RNF168 catalyzes H2A and H2AX ubiquitination on lysine 13/15 (K13/K15) upon DNA damage and promotes the accrual of downstream repair factors at damaged chromatin. Here, we report that RNF168 ubiquitinates the non-canonical H2A variants H2AZ and macroH2A1/2 at the divergent N-terminal tail lysine residue. In addition to their evolutionarily conserved nucleosome acidic patch, we identify the positively charged alpha1-extension helix as essential for RNF168-mediated ubiquitination of H2A variants. Moreover, mutation of the RNF168 UMI (UIM- and MIU-related UBD) hydrophilic acidic residues abolishes RNF168-mediated ubiquitination as well as 53BP1 and BRCA1 ionizing radiation-induced foci formation. Our results reveal a juxtaposed bipartite electrostatic interaction utilized by the nucleosome to direct RNF168 orientation towards the target lysine residues in proximity to the H2A alpha1-extension helix, which plays an important role in the DDR pathway.

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Structural basis of specific H2A K13/K15 ubiquitination by RNF168.

Project description:Ubiquitination of chromatin by modification of histone H2A is a critical step in both regulation of DNA repair and regulation of cell fate. These very different outcomes depend on the selective modification of distinct lysine residues in H2A, each by a specific E3 ligase. While polycomb PRC1 complexes modify K119, resulting in gene silencing, the E3 ligase RNF168 modifies K13/15, which is a key event in the response to DNA double-strand breaks. The molecular origin of ubiquitination site specificity by these related E3 enzymes is one of the open questions in the field. Using a combination of NMR spectroscopy, crosslinking mass-spectrometry, mutagenesis and data-driven modelling, here we show that RNF168 binds the acidic patch on the nucleosome surface, directing the E2 to the target lysine. The structural model highlights the role of E3 and nucleosome in promoting ubiquitination and provides a basis for understanding and engineering of chromatin ubiquitination specificity.

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