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Real-Time Monitoring and Modulation of Blood Pressure in a Rabbit Model of Ischemic Stroke
Published on: February 10, 2023
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OCT4B-190 protects against ischemic stroke by modulating GSK-3β/HDAC6
Yanting Chen1, Zhengzheng Wu2, Xiaolei Zhu1
1Department of Neurology, Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing 210008, China; Institute of Brain Science, Nanjing University, Nanjing 210008, China.
Experimental Neurology
|April 15, 2019
Summary
The OCT4B-190 protein isoform offers neuroprotection against stroke by modulating GSK-3β and HDAC6 activity, potentially serving as a novel therapeutic target for ischemic stroke.
Area of Science:
- Neuroscience
- Molecular Biology
- Stem Cell Biology
Background:
- OCT4 is crucial for embryonic stem cell pluripotency.
- OCT4B-190, a protein isoform of OCT4B mRNA, has an undefined biological function.
- Glycogen synthase kinase-3β (GSK-3β) and histone deacetylase 6 (HDAC6) are key stress modulators in stroke.
Purpose of the Study:
- To investigate the neuroprotective effects of OCT4B-190 in experimental stroke models.
- To explore the roles of GSK-3β and HDAC6 in OCT4B-190-mediated neuroprotection.
Main Methods:
- In vitro studies using oxygen-glucose deprivation (OGD) on neuronal cultures.
- In vivo studies using middle cerebral artery occlusion (MCAO) in male C57BL/6 mice.
- Adenovirus-mediated OCT4B-190 overexpression and analysis of GSK-3β and HDAC6 activity and expression.
Main Results:
- OCT4B-190 overexpression enhanced neuronal viability post-OGD.
- In MCAO mice, OCT4B-190 overexpression reduced infarct volume and improved neurological function.
- OCT4B-190 modulated GSK-3β activity and HDAC6 expression, affecting their interaction in neurons.
Conclusions:
- OCT4B-190 demonstrates significant neuroprotection in experimental stroke.
- OCT4B-190 likely exerts its effects by simultaneously regulating GSK-3β and HDAC6.
- OCT4B-190 represents a potential therapeutic strategy for ischemic stroke.
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