Expression of chemokine-like factor 1 after focal cerebral ischemia in the rat

► Focal cerebral ischemia resulted in an increased expression of several cytokines. ► Increase of CKLF1 expression in the ischemic cortex and hippocampus. ► CKLF1 mainly present in the cortex, hippocampus, thalamus and hypothalamus. ► CKLF1 may be an important regulator for cerebral ischemia. Cerebr...

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Bibliographic Details
Published in:Neuroscience letters 2011-11, Vol.505 (1), p.14-18
Main Authors: Kong, Ling-Lei, Hu, Jin-Feng, Zhang, Wei, Yuan, Yu-He, Ma, Kai-Li, Han, Ning, Chen, Nai-Hong
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Brain - metabolism
Brain - pathology
Cerebral ischemia
Chemokine-like factor 1
Chemokines - genetics
Chemokines - metabolism
Disease Models, Animal
Functional Laterality - physiology
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation - physiology
Infarction, Middle Cerebral Artery - pathology
Infarction, Middle Cerebral Artery - physiopathology
Inflammation
Male
MARVEL Domain-Containing Proteins
Medical sciences
Neurology
Rats
Rats, Sprague-Dawley
RNA, Messenger - metabolism
Vascular diseases and vascular malformations of the nervous system
Vertebrates: nervous system and sense organs
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Summary:► Focal cerebral ischemia resulted in an increased expression of several cytokines. ► Increase of CKLF1 expression in the ischemic cortex and hippocampus. ► CKLF1 mainly present in the cortex, hippocampus, thalamus and hypothalamus. ► CKLF1 may be an important regulator for cerebral ischemia. Cerebral ischemic injury is associated with the induction of a series of pro-inflammatory mediators such as cytokines and chemokines. The chemokine-like factor 1(CKLF1), as a novel human cytokine, displays chemotactic activities in a wide spectrum of leukocytes. The present study was conducted to determine if CKLF1 was produced in the brain of rats subjected to transient middle cerebral artery occlusion (TMCAO). Therefore, RT-PCR, Western blot and immunohistochemistry were utilized to characterize the expression of CKLF1 at different times after TMCAO. The result showed that almost no expression of CKLF1 was found in the sham-operated or contralateral cerebral cortex and hippocampus. CKLF1 expression significantly increased in the ischemic cerebral cortex and hippocampus, elevating at 12 h and peaking at 2 days after reperfusion. CKLF1 positive staining was mainly present in the cerebral cortex, hippocampus, thalamus, and hypothalamus. These results demonstrate that the expression of CKLF1 increases after focal cerebral ischemia in rat brain. Thus, CKLF1 may be a potential therapeutic target for cerebral ischemia.
ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2011.09.031