title: Overexpression Bax interacting factor-1 protects cortical neurons against cerebral ischemia-reperfusion injury through regulation of ERK1/2 pathway.
abstract: Bax interacting factor-1 (Bif-1), a multifunctional protein, can regulate cell apoptosis and autophagy. Up-regulation of Bif-1 expression has been associated with neuronal survival. Moreover, several studies have reported that Bif-1 is involved in ischemic stroke. However, the specific function of Bif-1 in cerebral ischemia-reperfusion (I/R) injury is not well understood. The aim of this study is to expose the potential protective effect of Bif-1 against cerebral I/R injury and its related mechanism. In the current study, we showed that adenovirus-mediated Bif-1-overexpression promoted oxygen and glucose deprivation followed by reperfusion (OGD/R)-treated cortical neurons' survival and reduced the cell apoptotic rate. We found that caspase-3 activity was inhibited by Bif-1 overexpression. In addition, we observed that Bif-1 overexpression induces cell autophagy, and the autophagy-specific inhibitor 3-Methyladenine (3-MA) attenuates cell survival. Interestingly, knockdown of Bif-1 resulted in attenuation of neuron survival, promotion of cell apoptosis and suppression of cell autophagy in neurons. In addition, knockdown of Bif-1 inhibited ERK1/2 activation. Our observations implicated Bif-1 as a novel target of cerebral I/R injury and played a neuroprotective effect via promoting cell survival and reducing apoptosis.
authors.affiliation: Department of Neurosurgery, Chinese PLA General Hospital, Beijing 100853, China; Department of Neurosurgery, Inner Mongolia People's Hospital, Hohhot 010020, China.
authors.forename: Qiang
authors.initials: Q
authors.lastname: Yun
authors.affiliation: Department of Neurology, Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, China.
authors.forename: Mingfang
authors.initials: M
authors.lastname: Jiang
authors.affiliation: Department of Neurology, Chinese PLA General Hospital, Beijing 100853, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Neurology, Chinese PLA General Hospital, Beijing 100853, China.
authors.forename: Xiangyu
authors.initials: X
authors.lastname: Cao
authors.affiliation: Department of Neurology, Chinese PLA General Hospital, Beijing 100853, China.
authors.forename: Xinfeng
authors.initials: X
authors.lastname: Liu
authors.affiliation: Department of Neurology, Chinese PLA General Hospital, Beijing 100853, China.
authors.forename: Sheng
authors.initials: S
authors.lastname: Li
authors.affiliation: Department of Neurology, Chinese PLA General Hospital, Beijing 100853, China. Electronic address: bmlixian@gmail.com.
authors.forename: Baomin
authors.initials: B
authors.lastname: Li
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000096:biosynthesis*; D000818:Animals; D000831:Animals, Newborn; D002545:Brain Ischemia / Q000378:metabolism* / Q000517:prevention & control; D002470:Cell Survival / Q000502:physiology; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000378:metabolism*; D005786:Gene Expression Regulation; D020935:MAP Kinase Signaling System / Q000502:physiology*; D009474:Neurons / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism* / Q000517:prevention & control
chemical_list: D048868:Adaptor Proteins, Signal Transducing; C429293:SH3GLB1 protein, human
keywords: Apoptosis; Bax interacting factor-1; Cerebral ischemia/reperfusion injury; ERK1/2; Survival