Hypoxia induces hypomethylation of the &amp;lt;italic&amp;gt;HMGB1&amp;lt;/italic&amp;gt; promoter via the MAPK/&amp;lt;italic&amp;gt;DNMT1&amp;lt;/italic&amp;gt;/&amp;lt;italic&amp;gt;HMGB1&amp;lt;/italic&amp;gt; pathway in cardiac progenitor cells

Su, Jinwen; Fang, Ming; Tian, Baohong; Luo, Jun; Jin, Can; Wang, Xuejun; Ning, Zhongping; Li, Xinming

doi:10.1093/abbs/gmy118

Cited by 6 publications

(5 citation statements)

References 31 publications

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“…Additionally, the MAPK signaling pathway is also involved in regulating the mechanism of post-hypoxic apoptosis of CPCs mediated by HMGB1. This study identified an important role of the MAPKs/DNMT1/HMGB1 signaling axis in regulating post-hypoxic apoptosis of CPCs and provided a new direction for CPCs apoptosis and proliferation, contributing to the development of valuable targets for stem cell therapy after MI ( Su et al, 2018 ).…”

Section: Roles Of Dna Methylation After Myocardial Infarctionmentioning

confidence: 95%

“…These cells can differentiate into cardiomyocytes, endothelial cells, and vascular smooth muscle cells, playing a significant role in protecting the heart and generating blood vessels to prevent adverse cardiac remodeling after MI ( Beltrami et al, 2003 ; Matsuura et al, 2009 ; van Berlo et al, 2014 ; Liu et al, 2015 ). However, after MI, the population of distinct cardiac side-population cells is reduced to less than half of their original levels 1 day after the injury, and only a few CPCs remain once large numbers are transplanted to the injured heart ( Mouquet et al, 2005 ; Su et al, 2018 ). Moreover, patients who suffered from MI showed higher levels of serum HMGB1, a protein closely related to inflammatory response, cell proliferation, and apoptosis ( Bell et al, 2006 ; Goldstein et al, 2006 ; Gwak et al, 2012 ; Kang et al, 2014 ).…”

Section: Roles Of Dna Methylation After Myocardial Infarctionmentioning

confidence: 99%

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A review on regulation of DNA methylation during post-myocardial infarction

Han,

Wang,

Wang

et al. 2024

Front. Pharmacol.

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Myocardial infarction (MI) imposes a huge medical and economic burden on society, and cardiac repair after MI involves a complex series of processes. Understanding the key mechanisms (such as apoptosis, autophagy, inflammation, and fibrosis) will facilitate further drug development and patient treatment. Presently, a substantial body of evidence suggests that the regulation of epigenetic processes contributes to cardiac repair following MI, with DNA methylation being among the notable epigenetic factors involved. This article will review the research on the mechanism of DNA methylation regulation after MI to provide some insights for future research and development of related drugs.

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Section: Roles Of Dna Methylation After Myocardial Infarctionmentioning

confidence: 95%

Section: Roles Of Dna Methylation After Myocardial Infarctionmentioning

confidence: 99%

A review on regulation of DNA methylation during post-myocardial infarction

Han,

Wang,

Wang

et al. 2024

Front. Pharmacol.

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“…Interestingly, the activation of the microglia, along with depressive symptoms, could be prevented by minocycline or imipramine [ 124 ]. While HMGB1 is a well-known marker of inflammation, increased expression of HMGB1 , associated with its promoter DNA’s methylation alteration, was reported in cardiac progenitor cells following hypoxia and metabolic diseases [ 79 , 80 ], suggesting that DNA methylation is a mechanism for HMGB1 regulation. However, in brain cells, HMGB1 expression is also regulated by HDAC4&5 and miR-129 [ 81 , 82 ], the latter of which was shown to regulate neuronal migration in mice brains [ 125 ].…”

Section: Astroglia Pathology and Dysfunction In Depressionmentioning

confidence: 99%

Epigenetic Alterations of Brain Non-Neuronal Cells in Major Mental Diseases

Abdolmaleky

Martin

Zhou

et al. 2023

Genes

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The tissue-specific expression and epigenetic dysregulation of many genes in cells derived from the postmortem brains of patients have been reported to provide a fundamental biological framework for major mental diseases such as autism, schizophrenia, bipolar disorder, and major depression. However, until recently, the impact of non-neuronal brain cells, which arises due to cell-type-specific alterations, has not been adequately scrutinized; this is because of the absence of techniques that directly evaluate their functionality. With the emergence of single-cell technologies, such as RNA sequencing (RNA-seq) and other novel techniques, various studies have now started to uncover the cell-type-specific expression and DNA methylation regulation of many genes (e.g., TREM2, MECP2, SLC1A2, TGFB2, NTRK2, S100B, KCNJ10, and HMGB1, and several complement genes such as C1q, C3, C3R, and C4) in the non-neuronal brain cells involved in the pathogenesis of mental diseases. Additionally, several lines of experimental evidence indicate that inflammation and inflammation-induced oxidative stress, as well as many insidious/latent infectious elements including the gut microbiome, alter the expression status and the epigenetic landscapes of brain non-neuronal cells. Here, we present supporting evidence highlighting the importance of the contribution of the brain’s non-neuronal cells (in particular, microglia and different types of astrocytes) in the pathogenesis of mental diseases. Furthermore, we also address the potential impacts of the gut microbiome in the dysfunction of enteric and brain glia, as well as astrocytes, which, in turn, may affect neuronal functions in mental disorders. Finally, we present evidence that supports that microbiota transplantations from the affected individuals or mice provoke the corresponding disease-like behavior in the recipient mice, while specific bacterial species may have beneficial effects.

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“…Although there is evidence that HMGB1 expression is regulated by DNA methylation in metabolic disease [59,60], there are no such studies in neurodegenerative diseases. However, a number of studies have shown that HMGB1 expression is regulated by HDAC4&5 and miR-129 in brain cells [61,62].…”

Section: Neuroinflammation and Microglia Dysregulated Genes In Ad And...mentioning

confidence: 99%

Underlying Mechanisms of Brain Aging and Neurodegenerative Diseases as Potential Targets for Preventive or Therapeutic Strategies Using Phytochemicals

Abdolmaleky

Zhou

2023

Nutrients

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During aging, several tissues and biological systems undergo a progressive decline in function, leading to age-associated diseases such as neurodegenerative, inflammatory, metabolic, and cardiovascular diseases and cancer. In this review, we focus on the molecular underpinning of senescence and neurodegeneration related to age-associated brain diseases, in particular, Alzheimer’s and Parkinson’s diseases, along with introducing nutrients or phytochemicals that modulate age-associated molecular dysfunctions, potentially offering preventive or therapeutic benefits. Based on current knowledge, the dysregulation of microglia genes and neuroinflammation, telomere attrition, neuronal stem cell degradation, vascular system dysfunction, reactive oxygen species, loss of chromosome X inactivation in females, and gut microbiome dysbiosis have been seen to play pivotal roles in neurodegeneration in an interactive manner. There are several phytochemicals (e.g., curcumin, EGCG, fucoidan, galangin, astin C, apigenin, resveratrol, phytic acid, acacetin, daucosterol, silibinin, sulforaphane, withaferin A, and betulinic acid) that modulate the dysfunction of one or several key genes (e.g., TREM2, C3, C3aR1, TNFA, NF-kb, TGFB1&2, SIRT1&6, HMGB1, and STING) affected in the aged brain. Although phytochemicals have shown promise in slowing down the progression of age-related brain diseases, more studies to identify their efficacy, alone or in combinations, in preclinical systems can help to design novel nutritional strategies for the management of neurodegenerative diseases in humans.

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Hypoxia induces hypomethylation of the <italic>HMGB1</italic> promoter via the MAPK/<italic>DNMT1</italic>/<italic>HMGB1</italic> pathway in cardiac progenitor cells

Cited by 6 publications

References 31 publications

A review on regulation of DNA methylation during post-myocardial infarction

A review on regulation of DNA methylation during post-myocardial infarction

Epigenetic Alterations of Brain Non-Neuronal Cells in Major Mental Diseases

Underlying Mechanisms of Brain Aging and Neurodegenerative Diseases as Potential Targets for Preventive or Therapeutic Strategies Using Phytochemicals

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