Hck Promotes Neuronal Apoptosis Following Intracerebral Hemorrhage
Male
Neurons
Rats, Sprague-Dawley
0301 basic medicine
03 medical and health sciences
Cell Line, Tumor
Proto-Oncogene Proteins c-hck
Animals
Humans
Apoptosis
Cerebral Hemorrhage
Rats
DOI:
10.1007/s10571-016-0365-0
Publication Date:
2016-04-06T07:03:41Z
AUTHORS (8)
ABSTRACT
The hematopoietic cell kinase (Hck) is a member of the Src family protein kinases which regulates many signal transduction pathways including cell growth, proliferation, differentiation, migration, and apoptosis. However, the expression and function of Hck after intracerebral hemorrhage (ICH) are unknown. Western blot, immunohistochemistry, and immunofluorescence showed that Hck was obviously up-regulation in neurons adjacent to the hematoma after ICH. In addition, the temporary raise of Hck expression was paralleled with the expression of p53, Bax, and active caspase-3, suggesting that Hck was involved in neuronal apoptosis. Hck siRNA dramatically decrease hemin-induced expression of p53, Bax, and active caspase-3 as well as the amount of apoptotic SH-SY5Y cells in vitro. Furthermore, Hck interacted with p53. Hence, Hck might promote neuronal apoptosis via p53 signaling pathway after ICH.
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