The inhibition of Cdk5 activity after hypoxia/ischemia injury reduces infarct size and promotes functional recovery in neonatal rats

Highlights • Cdk5 activity increases after hypoxia/ischemia injury accompanying with the increase of p25 level. • P35 mimetic peptide p5-TAT interacts with Cdk5 and inhibits Cdk5 activity after hypoxia/ischemia injury. • P5-TAT treatment reduces infarct volume and promotes the neurological functiona...

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Veröffentlicht in:	Neuroscience 2015-04, Vol.290, p.552-560
Hauptverfasser:	Tan, X, Chen, Y, Li, J, Li, X, Miao, Z, Xin, N, Zhu, J, Ge, W, Feng, Y, Xu, X
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Animals, Newborn apoptosis Brain - drug effects Brain - pathology Brain - physiopathology Caspase 3 - metabolism Cdk5 Cyclin-Dependent Kinase 5 - antagonists & inhibitors Cyclin-Dependent Kinase 5 - metabolism Disease Models, Animal Hypoxia-Ischemia, Brain - drug therapy Hypoxia-Ischemia, Brain - pathology Hypoxia-Ischemia, Brain - physiopathology hypoxia/ischemia injury Nerve Tissue Proteins - metabolism Neurology Neuroprotective Agents - pharmacology p35 p35 mimetic peptide Phosphorylation - drug effects Phosphotransferases - antagonists & inhibitors Phosphotransferases - metabolism Random Allocation Rats, Sprague-Dawley Receptors, Glucocorticoid - metabolism Recovery of Function - drug effects Recovery of Function - physiology tau Proteins - metabolism
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Zusammenfassung:	Highlights • Cdk5 activity increases after hypoxia/ischemia injury accompanying with the increase of p25 level. • P35 mimetic peptide p5-TAT interacts with Cdk5 and inhibits Cdk5 activity after hypoxia/ischemia injury. • P5-TAT treatment reduces infarct volume and promotes the neurological functional recovery.
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2015.01.054