title: p63 Expression in the Gerbil Hippocampus Following Transient Ischemia and Effect of Ischemic Preconditioning on p63 Expression in the Ischemic Hippocampus.
abstract: p63 is a transcription factor of p53 gene family, which are involved in development, differentiation and cell response to stress; however, its roles in ischemic preconditioning (IPC) in the brain are not clear. In the present study, we investigated the effect of IPC on p63 immunoreactivity caused by 5 min of transient cerebral ischemia in gerbils. IPC was induced by subjecting the gerbils to 2 min of transie ischemia 1 day prior to 5 min of transient ischemia. The animals were randomly assigned to four groups (sham-operated-group, ischemia-operated-group, IPC plus (+)-sham-operated-group and IPC + ischemia-operated-group). The number of viable neurons in the stratum pyramidale of the hippocampal CA1 region (CA1) was significantly increased by IPC + ischemia-operated-group compared with that in the ischemia-operated-group 5 days after ischemic insult. We found that strong p63 immunoreactivity was detected in the CA1 pyramidal neurons in the sham-operated-group, and the immunoreactivity was decreased with time after ischemia-reperfusion. In addition, strong p63 immunoreactivity was newly expressed in microglial cells of the CA1 region from 2 days after ischemia-reperfusion. In all the IPC + sham-operated-groups, p63 immunoreactivity in the CA1 pyramidal neurons was similar to that in the sham-operated-group, and the immunoreactivity was well maintained in the IPC + ischemia-operated-groups after cerebral ischemia. In brief, our present findings show that IPC dramatically protected the reduction of p63 immunoreactivity in the pyramidal neurons of the CA1 region after ischemia-reperfusion, and this result suggests that the expression of p63 may be necessary for neurons to survive after transient cerebral ischemia.
authors.affiliation: Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea.
authors.forename: Jae-Chul
authors.initials: JC
authors.lastname: Lee
authors.forename: Geum-Sil
authors.initials: GS
authors.lastname: Cho
authors.forename: In Hye
authors.initials: IH
authors.lastname: Kim
authors.forename: Joon Ha
authors.initials: JH
authors.lastname: Park
authors.forename: Jeong-Hwi
authors.initials: JH
authors.lastname: Cho
authors.forename: Ji Hyeon
authors.initials: JH
authors.lastname: Ahn
authors.forename: Eun Joo
authors.initials: EJ
authors.lastname: Bae
authors.forename: Ji Yun
authors.initials: JY
authors.lastname: Ahn
authors.forename: Chan Woo
authors.initials: CW
authors.lastname: Park
authors.forename: Jun Hwi
authors.initials: JH
authors.lastname: Cho
authors.forename: Young-Myeong
authors.initials: YM
authors.lastname: Kim
authors.forename: Moo-Ho
authors.initials: MH
authors.lastname: Won
authors.forename: Hui Young
authors.initials: HY
authors.lastname: Lee
mesh_terms: D000818:Animals; D056547:CA1 Region, Hippocampal / Q000378:metabolism* / Q000473:pathology; D005786:Gene Expression Regulation; D005849:Gerbillinae; D002546:Ischemic Attack, Transient / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control*; D019194:Ischemic Preconditioning / Q000379:methods*; D008297:Male; D010750:Phosphoproteins / Q000096:biosynthesis*; D015534:Trans-Activators / Q000096:biosynthesis*
chemical_list: D010750:Phosphoproteins; D015534:Trans-Activators; C486419:Trp63 protein, mouse