1
40
3
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Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1074/jbc.M113.512269" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M113.512269</a>
Pages
6877–6885
Issue
10
Volume
289
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Modulation of ten-eleven translocation 1 (TET1), Isocitrate Dehydrogenase (IDH) expression, alpha-Ketoglutarate (alpha-KG), and DNA hydroxymethylation levels by interleukin-1beta in primary human chondrocytes.
Publisher
An entity responsible for making the resource available
The Journal of biological chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-03
Subject
The topic of the resource
*DNA Methylation; *Epigenesis; 5-hmC; 5-Methylcytosine/analogs & derivatives; Chondrocytes; Chondrocytes/chemistry/*metabolism; Cytokine; Cytosine/*analogs & derivatives/analysis/metabolism; Dioxygenase; DNA Methylation; DNA-Binding Proteins/*biosynthesis/genetics; Epigenetics; Genetic; Humans; IL-1; Interleukin-1beta/pharmacology/*physiology; Isocitrate Dehydrogenase/*biosynthesis/genetics; Ketoglutaric Acids/*metabolism; Messenger/biosynthesis/genetics; Mixed Function Oxygenases; Primary Cell Culture; Proto-Oncogene Proteins/*biosynthesis/genetics; RNA; TNF-alpha; Tumor Necrosis Factor-alpha/pharmacology/physiology
Creator
An entity primarily responsible for making the resource
Haseeb Abdul; Makki Mohammad Shahidul; Haqqi Tariq M
Description
An account of the resource
5-Hydroxymethylcytosine (5-hmC) generated by ten-eleven translocation 1-3 (TET1-3) enzymes is an epigenetic mark present in many tissues with different degrees of abundance. IL-1beta and TNF-alpha are the two major cytokines present in arthritic joints that modulate the expression of many genes associated with cartilage degradation in osteoarthritis. In the present study, we investigated the global 5-hmC content, the effects of IL-1beta and TNF-alpha on 5-hmC content, and the expression and activity of TETs and isocitrate dehydrogenases in primary human chondrocytes. The global 5-hmC content was found to be approximately 0.1% of the total genome. There was a significant decrease in the levels of 5-hmC and the TET enzyme activity upon treatment of chondrocytes with IL-1beta alone or in combination with TNF-alpha. We observed a dramatic (10-20-fold) decrease in the levels of TET1 mRNA expression and a small increase (2-3-fold) in TET3 expression in chondrocytes stimulated with IL-1beta and TNF-alpha. IL-1beta and TNF-alpha significantly suppressed the activity and expression of IDHs, which correlated with the reduced alpha-ketoglutarate levels. Whole genome profiling showed an erasure effect of IL-1beta and TNF-alpha, resulting in a significant decrease in hydroxymethylation in a myriad of genes including many genes that are important in chondrocyte physiology. Our data demonstrate that DNA hydroxymethylation is modulated by pro-inflammatory cytokines via suppression of the cytosine hydroxymethylation machinery. These data point to new mechanisms of epigenetic control of gene expression by pro-inflammatory cytokines in human chondrocytes.
Identifier
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<a href="http://doi.org/10.1074/jbc.M113.512269" target="_blank" rel="noreferrer noopener">10.1074/jbc.M113.512269</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*DNA methylation
*Epigenesis
2014
5-hmC
5-Methylcytosine/analogs & derivatives
Chondrocytes
Chondrocytes/chemistry/*metabolism
Cytokine
Cytosine/*analogs & derivatives/analysis/metabolism
Department of Anatomy & Neurobiology
Dioxygenase
DNA Methylation
DNA-Binding Proteins/*biosynthesis/genetics
Epigenetics
Genetic
Haqqi Tariq M
Haseeb Abdul
Humans
IL-1
Interleukin-1beta/pharmacology/*physiology
Isocitrate Dehydrogenase/*biosynthesis/genetics
Ketoglutaric Acids/*metabolism
Makki Mohammad Shahidul
Messenger/biosynthesis/genetics
Mixed Function Oxygenases
NEOMED College of Medicine
Primary Cell Culture
Proto-Oncogene Proteins/*biosynthesis/genetics
RNA
The Journal of biological chemistry
TNF-alpha
Tumor Necrosis Factor-alpha/pharmacology/physiology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.ijcard.2018.05.058" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ijcard.2018.05.058</a>
Pages
193–194
Volume
268
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Epigenetic regulation in diabetes-associated oxidative stress and myocardial dysfunction.
Publisher
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International journal of cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-10
Subject
The topic of the resource
*Epigenesis; *Oxidative Stress; Cardiomyopathies; Genetic; Humans
Creator
An entity primarily responsible for making the resource
Yin Liya; Chilian William M; Dong Feng
Identifier
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<a href="http://doi.org/10.1016/j.ijcard.2018.05.058" target="_blank" rel="noreferrer noopener">10.1016/j.ijcard.2018.05.058</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Epigenesis
*Oxidative Stress
2018
Cardiomyopathies
Chilian William M
Department of Integrative Medical Sciences
Dong Feng
Genetic
Humans
International journal of cardiology
NEOMED College of Medicine
Yin Liya
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.bbadis.2017.11.004" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.bbadis.2017.11.004</a>
Pages
432–443
Issue
2
Volume
1864
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Epigenetic regulation of astrocyte function in neuroinflammation and neurodegeneration.
Publisher
An entity responsible for making the resource available
Biochimica et biophysica acta. Molecular basis of disease
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-02
Subject
The topic of the resource
*Astrocyte; *DNA methylation; *Epigenesis; *Epigenetic; *Histone; *Neurodegeneration; *Neuroinflammation; Acetylation; Alzheimer Disease/genetics/pathology; Animals; Astrocytes/*cytology/immunology; Cell Differentiation; DNA Methylation; Genetic; Histones/metabolism; Humans; Inflammation/*pathology; Methylation; MicroRNAs/metabolism; Neurodegenerative Diseases/genetics/*pathology; Neuroglia/metabolism; Neurons/immunology; Parkinson Disease/genetics/pathology
Creator
An entity primarily responsible for making the resource
Neal Matthew; Richardson Jason R
Description
An account of the resource
Epigenetic mechanisms control various functions throughout the body, from cell fate determination in development to immune responses and inflammation. Neuroinflammation is one of the prime contributors to the initiation and progression of neurodegeneration in a variety of diseases, including Alzheimer's and Parkinson's diseases. Because astrocytes are the largest population of glial cells, they represent an important regulator of CNS function, both in health and disease. Only recently have studies begun to identify the epigenetic mechanisms regulating astrocyte responses in neurodegenerative diseases. These epigenetic mechanisms, along with the epigenetic marks involved in astrocyte development, could elucidate novel pathways to potentially modulate astrocyte-mediated neuroinflammation and neurotoxicity. This review examines the known epigenetic mechanisms involved in regulation of astrocyte function, from development to neurodegeneration, and links these mechanisms to potential astrocyte-specific roles in neurodegenerative disease with a focus on potential opportunities for therapeutic intervention.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.bbadis.2017.11.004" target="_blank" rel="noreferrer noopener">10.1016/j.bbadis.2017.11.004</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Astrocyte
*DNA methylation
*Epigenesis
*Epigenetic
*Histone
*neurodegeneration
*Neuroinflammation
2018
Acetylation
Alzheimer Disease/genetics/pathology
Animals
Astrocytes/*cytology/immunology
Biochimica et biophysica acta. Molecular basis of disease
Cell Differentiation
Department of Pharmaceutical Sciences
DNA Methylation
Genetic
Histones/metabolism
Humans
Inflammation/*pathology
Methylation
MicroRNAs/metabolism
Neal Matthew
NEOMED College of Pharmacy
Neurodegenerative Diseases/genetics/*pathology
Neuroglia/metabolism
Neurons/immunology
Parkinson Disease/genetics/pathology
Richardson Jason R