p39 Affects Myelin Formation in Cerebral Ischemic Injury.

Autor: Meng D; Department of Neurology and Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou, China.; Department of Neurology, Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, China., Wu D; Department of Neurology, Nanjing Jinling Hospital, Nanjing, China., Li X; Suzhou Hospital, Affiliated Hospital of Medical School, Nanjing University, Suzhou, China. lixiaojing_chen@163.com., Miao Z; Department of Neurology and Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou, China. zgmiao@suda.edu.cn.; Institute of Neuroscience of Soochow University, 199 Ren-Ai Road, Suzhou City, 215123, China. zgmiao@suda.edu.cn.
Jazyk: angličtina
Zdroj: Neuromolecular medicine [Neuromolecular Med] 2024 Jun 01; Vol. 26 (1), pp. 22. Date of Electronic Publication: 2024 Jun 01.
DOI: 10.1007/s12017-024-08792-3
Abstrakt: Stroke is a significant public health issue, and research has consistently focused on studying the mechanisms of injury and identifying new targets. As a CDK5 activator, p39 plays a crucial role in various diseases. In this article, we will explore the role and mechanism of p39 in cerebral ischemic injury. We measured the level of p39 using western blot and QPCR at various time points following cerebral ischemia-reperfusion (I/R) injury. The results indicated a significant reduction in the level of p39. TTC staining and behavioral results indicate that the knockout of p39 (p39KO) provides neuroprotection in the short-term. Interestingly, the behavioral dysfunction in p39KO mice was exacerbated after the repair phase of I/R. Further study revealed that this deterioration may be due to demyelination induced by elevated p35 levels. In summary, our study offers profound insights into the significance of p39 in both the acute and repair stages of ischemic injury recovery and a theoretical foundation for future therapeutic drug exploration.
(© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze: MEDLINE
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