Histochemical mapping of hnRNP A2/B1 in rat brain after ischemia-reperfusion insults.
Cerebral ischemia-reperfusion (I/R) insults result in neuronal cell death, brain tissue loss, and severe neurological deficits. However, the underlying mechanism is still not fully understood. Heterogeneous nuclear ribonucleoprotein (hnRNP) A2/B1 belongs to a family of RNA-binding proteins that plays a central role in pre-mRNA processing. Recent studies have revealed that hnRNP A2/B1 may be involved in the progress of I/R; therefore, the present study aimed to examine expression patterns of hnRNP A2/B1 to better understand posttranscriptional regulations in cerebral I/R insults. Focal cerebral I/R models were induced by right middle cerebral artery occlusion (MCAO) for 120 min followed by 3, 6, 12, 24, 48, and 72 hr of reperfusion in male Sprague-Dawley rats. We employed immunohistochemistry to examine expression of hnRNP A2/B1 in rat cerebral cortex (including cingulate cortex, striate cortex, temporal cortex, and piriform cortex) and hippocampus after I/R insults. Results showed that expression of hnRNP A2/B1 was significantly downregulated in cerebral cortex and hippocampus from 3 to 24 hr of reperfusion after MCAO for 120 min, but significantly upregulated at 48 hr of reperfusion. Unexpectedly, translocation of hnRNP A2/B1 from nucleus to cytoplasm and even to neurites was observed in cerebral cortex at 3 hr of reperfusion, reaching a peak at 24 hr of reperfusion, but not in hippocampus, indicating different posttranscriptional regulation patterns in different brain regions. Interestingly, translocation of hnRNP A2/B1 was only observed in cerebral cortex with MCAO but not in the opposite side, suggesting an I/R-specific expression pattern in the brain. Our data suggest that hnRNP A2/B1 participates in posttranscriptional regulation of neurons in cerebral cortex and hippocampus that suffered I/R insults, although posttranscriptional regulation is more extensive in neuronal cells of cerebral cortex than in hippocampus.
Liu
Yichen
Y
Beijing Institute of Radiation Medicine, State Key Laboratory of Proteomics, Beijing, China.
Gao
Yan
Y
Wu
Yan
Y
Wu
Yonghong
Y
Wang
Hangyan
H
Zhang
Chenggang
C
D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology*; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology; D005786:Gene Expression Regulation; D034481:Heterogeneous-Nuclear Ribonucleoprotein Group A-B / Q000032:analysis / Q000235:genetics / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D008297:Male; D020768:Middle Cerebral Artery / Q000378:metabolism; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D021381:Protein Transport; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000473:pathology*
D034481:Heterogeneous-Nuclear Ribonucleoprotein Group A-B