Premium
Expression of the Apoptosis‐Effector Gene, Bax, Is Up‐Regulated in Vulnerable Hippocampal CA1 Neurons Following Global Ischemia
Author(s) -
Chen Jun,
Zhu Raymond L.,
Nakayama Masaki,
Kawaguchi Kenji,
Jin Kunlin,
Stetler R. Anne,
Simon Roger P.,
Graham Steven H.
Publication year - 1996
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1996.67010064.x
Subject(s) - effector , programmed cell death , hippocampal formation , dentate gyrus , apoptosis , ischemia , biology , microbiology and biotechnology , bcl 2 family , messenger rna , gene expression , gene , bcl 2 associated x protein , neuroscience , genetics , medicine , caspase 3
The observation that delayed death of CA1 neurons after global ischemia is inhibited by protein synthesis inhibitors suggests that the delayed death of these neurons is an active process that requires new gene expression. Delayed death in CA1 has some of the characteristics of apoptotic death; however, candidate proapoptotic proteins have not been identified in the CA1 after ischemia. We studied the expression of Bax protein and mRNA, a member of the bcl‐2 family that is an effector of apoptotic cell death, after global ischemia in the four‐vessel global ischemia model in the rat and compared these results with the expression of the antiapoptotic gene bcl‐2 . Bax mRNA and protein are both expressed in CA1 before delayed death, whereas bcl‐2 protein is not expressed. Bcl‐2 protein expression, but not that of Bax, is increased in CA3, a region that is ischemic but less susceptible to ischemic injury. In the dentate gyrus, both Bax and bcl‐2 proteins are expressed. The selective expression of Bax in CA1 supports the hypothesis that Bax could contribute to delayed neuronal death in these vulnerable neurons by an independent mechanism or by forming heterodimers with gene family members other than bcl‐2.