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The Detection of 5-Hydroxymethylcytosine in Neural Stem Cells and Brains of Mice
Published on: September 19, 2019
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Altering 5-hydroxymethylcytosine modification impacts ischemic brain injury
Zhigang Miao1, Yuquan He2, Ning Xin3
1Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Department of Neurology, The Second Affiliated Hospital of Soochow University, Suzhou City, Jiangsu Province 215004, P.R. China, Institute of Neuroscience, Soochow University, Suzhou City, Jiangsu Province 215123, P.R. China.
Human Molecular Genetics
|August 2, 2015
Summary
Increased 5-hydroxymethylcytosine (5hmC) levels after ischemic stroke, mediated by Tet2, indicate its potential as a therapeutic target and biomarker for stroke treatment.
Area of Science:
- Neuroscience
- Epigenetics
- Molecular Biology
Background:
- Epigenetic modifications, including DNA methylation, are crucial in ischemic brain injury.
- 5-hydroxymethylcytosine (5hmC) is an epigenetic mark involved in DNA methylation dynamics.
- Ten-eleven translocation (Tet) enzymes mediate the conversion of 5-methylcytosine to 5hmC.
Purpose of the Study:
- To investigate the role of 5hmC and Tet enzymes in ischemic brain injury.
- To identify potential epigenetic biomarkers and therapeutic targets for ischemic stroke.
Main Methods:
- Induction of ischemic injury in animal models.
- Measurement of 5hmC levels and Tet2 expression.
- Genome-wide profiling of 5hmC.
- Analysis of gene expression (mRNA and protein) for BDNF.
- Analysis of 5hmC levels in blood samples from stroke patients.
Main Results:
- 5hmC abundance significantly increased after ischemic injury, mediated by Tet2.
- Inhibition of Tet2 exacerbated infarct volume and reduced 5hmC levels.
- Differentially hydroxymethylated regions (DhMRs) were identified, enriched in genes related to neuronal function.
- 5hmC and BDNF expression increased in the injured brain, with Tet2 inhibition reducing BDNF.
- Elevated 5hmC levels were observed in blood samples from acute ischemic stroke patients.
Conclusions:
- Tet2-mediated 5hmC increase plays a role in the response to ischemic brain injury.
- 5hmC modifications are associated with key genes involved in neuronal plasticity and development.
- 5hmC in blood may serve as a biomarker for ischemic stroke.
- Targeting Tet2-mediated 5hmC pathways could offer a therapeutic strategy for ischemic stroke.
