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Expression of the RNA‐binding protein TIAR is increased in neurons after ischemic cerebral injury
Author(s) -
Jin Kunlin,
Li Wenjin,
Nagayama Tetsuya,
He Xiangjun,
Sinor Amy D.,
Chang Juni,
Mao Xiaoou,
Graham Steven H.,
Simon Roger P.,
Greenberg David A.
Publication year - 2000
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(20000315)59:6<767::aid-jnr9>3.0.co;2-k
Subject(s) - ischemia , cerebral cortex , microbiology and biotechnology , apoptosis , messenger rna , programmed cell death , biology , immunocytochemistry , immunofluorescence , intracellular , medicine , endocrinology , antibody , immunology , gene , biochemistry
T‐cell restricted intracellular antigen‐related protein (TIAR) is an RNA recognition motif‐type RNA‐binding protein that has been implicated in the apoptotic death of T‐lymphocytes and retinal pigment epithelial cells. Western blots prepared with a monoclonal antibody against TIAR showed expression in normal rat hippocampus, and induction by 15 min of global cerebral ischemia. This increased expression was evident at 8 hr after ischemia and maximal at 24 hr, whereas expression at 72 hr was reduced below basal levels. Expression of TIAR protein was also increased in parietal cortex 6 and 24 hr after 90 min of focal cerebral ischemia induced by middle cerebral artery (MCA) occlusion, as well as in cultured cortical neurons and astroglia after exposure to hypoxia in vitro. Immunocytochemistry showed that increased expression of TIAR occurred mainly in the CA1 sector of hippocampus 24 hr after global ischemia, and in cortical and striatal neurons 24 hr after 20 or 90 min of focal ischemia. Double‐labeling studies showed that TIAR protein expression was co‐localized with DNA damage in neuronal cells. The findings suggest that TIAR may be involved in neuronal cell death after cerebral ischemic injury. J. Neurosci. Res. 59:767–774, 2000 © 2000 Wiley‐Liss, Inc.