Phosphorylation of PYK2 and p38MAPK in neurons after focal cerebral ischemia in rats
- VernacularTitle:大鼠脑缺血后神经元中PYK2及p38MAPK的活化及其意义
- Author:
Xuemei LI
;
Junhong JIA
;
Wei REN
- Publication Type:Journal Article
- Keywords:
cerebral ischemia;
neurons;
p38 MAP kinase;
PYK2
- From:
Medical Journal of Chinese People's Liberation Army
1981;0(06):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate and evaluate the changes of phospho PYK2 and phospho p38MAPK expression in neurons after focal cerebral ischemia. Methods Focal ischemia reperfusion model was established in rats, and by using immunostaining, the changes of phospho PYK2 and phospho p38MAPK expression in neurons was observed. Results Faint phospho PYK2 and phospho p38MAPK immunoreactivity were revealed in normal cortical neurons. Fifteen minutes after the ischemia onset, a pronounced upregulation of phospho PYK2 and phospho p38MAPK immunoreactivities were evident in these ischemia attacked neurons. The immunoreactivities of phospho PYK2 and phospho p38MAPK reached its peak at 30min after ischemia, and decreased 60min after ischemia. Conclusion Cerebral ischemia was able to induce neuronal PYK2 phosphorylation. The activation of PYK2 might link ischemia attack to the p38MAPK signaling pathway to initiate the neuronal response to the stress stimuli
