title: Up-regulation of Che-1 relates to neuronal apoptosis after traumatic brain injury in adult rats.
abstract: Che-1, a recently identified apoptosis related protein, affects the fate of various cell types when under stress. One attractive biological function of Che-1 is promoting the transcription of p53 after DNA damage; besides, it can also regulate cell cycle via interacting with retinoblastoma protein. Although previous evidence has showed its anti-apoptotic role in cancer cells, some studies point out that Che-1 might play an opposite role in central nervous system (CNS). However, the function of Che-1 in CNS is still with limited acquaintance. To investigate whether Che-1 is involved in CNS lesion, we performed a traumatic brain injury model in adult rats. Up-regulation of Che-1 was observed in the peritrauma brain cortex by performing western blotting and immunohistochemistry. Terminal deoxynucleotidyl transferase deoxy-UTP nick-end labeling and 4',6-diamidino-2-phenylindole staining suggested that Che-1 was involved in neuronal apoptosis after brain injury. We also investigated co-localization of Che-1 and active-caspase-3 in the ipsilateral brain cortex. In addition, the expression patterns of p53, Bax and PCNA were parallel with that of Che-1. Besides this, neurotrophin receptor-interacting MAGE homolog was found to be associated with Che-1 after brain trauma. Based on our data, we suggested that Che-1 might play an important role in neuronal apoptosis following TBI; and might provide a basis for the further study on its role in regulating the expression of p53 and cell cycle re-entry in traumatic brain injury.
authors.affiliation: Department of Psychiatry, Affiliated Mental and Health Center of Nantong University, Nantong, 226001, Jiangsu Province, People's Republic of China.
authors.forename: Jian
authors.initials: J
authors.lastname: Xu
authors.forename: Wei
authors.initials: W
authors.lastname: Jin
authors.forename: Xinmin
authors.initials: X
authors.lastname: Wu
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Wu
authors.forename: Aihong
authors.initials: A
authors.lastname: Li
authors.forename: Kaifu
authors.initials: K
authors.lastname: Ke
authors.forename: Jianhua
authors.initials: J
authors.lastname: Cao
authors.forename: Xiaojuan
authors.initials: X
authors.lastname: Liu
authors.forename: Xiang
authors.initials: X
authors.lastname: Tan
authors.forename: Hongran
authors.initials: H
authors.lastname: Fu
authors.forename: Yilu
authors.initials: Y
authors.lastname: Gao
authors.forename: Zhiwei
authors.initials: Z
authors.lastname: Gao
mesh_terms: D000367:Age Factors; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology; D008297:Male; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D009687:Nuclear Proteins / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014157:Transcription Factors / Q000096:biosynthesis*; D015854:Up-Regulation / Q000502:physiology*
chemical_list: C523104:Aatf protein, rat; D009687:Nuclear Proteins; D014157:Transcription Factors