naa a22 4500 510775799 CHVBK 20180411083229.0 cr unu---uuuuu 180411e20131201xx s 000 0 eng 10.1007/s12975-013-0273-2 doi (NATIONALLICENCE)springer-10.1007/s12975-013-0273-2 HuR Function and Translational State Analysis Following Global Brain Ischemia and Reperfusion [Elektronische Daten] [Jeffrey Szymanski, Haihui Wang, Jill Jamison, Donald DeGracia] Prolonged translation arrest in post-ischemic hippocampal CA1 pyramidal neurons precludes translation of induced stress genes and directly correlates with cell death. We evaluated the regulation of mRNAs containing adenine- and uridine-rich elements (ARE) by assessing HuR protein and hsp70 mRNA nuclear translocation, HuR polysome binding, and translation state analysis of CA1 and CA3 at 8h of reperfusion after 10min of global cerebral ischemia. There was no difference between CA1 and CA3 at 8h of reperfusion in nuclear or cytoplasmic HuR protein or hsp70 mRNA, or HuR polysome association, suggesting that neither mechanism contributed to post-ischemic outcome. Translation state analysis revealed that 28 and 58% of unique mRNAs significantly different between 8hR and NIC, in CA3 and CA1, respectively, were not polysome-bound. There was significantly greater diversity of polysome-bound mRNAs in reperfused CA3 compared to CA1, and in both regions, ARE-containing mRNAs accounted for 4-5% of the total. These data indicate that posttranscriptional ARE-containing mRNA regulation occurs in reperfused neurons and contributes to post-ischemic outcome. Understanding the differential responses of vulnerable and resistant neurons to ischemia will contribute to the development of effective neuroprotective therapies. Springer Science+Business Media New York, 2013 CA1 nationallicence CA3 nationallicence Global cerebral ischemia nationallicence HSP70 nationallicence HuR nationallicence Microarray nationallicence Stress responses nationallicence Translation state analysis nationallicence Szymanski Jeffrey Department of Physiology, Wayne State University School of Medicine, 4116 Scott Hall, 540 East Canfield Ave, 48201, Detroit, MI, USA aut Wang Haihui Department of Physiology, Wayne State University School of Medicine, 4116 Scott Hall, 540 East Canfield Ave, 48201, Detroit, MI, USA aut Jamison Jill Department of Physiology, Wayne State University School of Medicine, 4116 Scott Hall, 540 East Canfield Ave, 48201, Detroit, MI, USA aut DeGracia Donald Department of Physiology, Wayne State University School of Medicine, 4116 Scott Hall, 540 East Canfield Ave, 48201, Detroit, MI, USA aut Translational Stroke Research Springer US; http://www.springer-ny.com 4/6(2013-12-01), 589-603 1868-4483 4:6<589 2013 4 12975 https://doi.org/10.1007/s12975-013-0273-2 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s12975-013-0273-2 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Szymanski Jeffrey Department of Physiology, Wayne State University School of Medicine, 4116 Scott Hall, 540 East Canfield Ave, 48201, Detroit, MI, USA aut NATIONALLICENCE 700 1- Wang Haihui Department of Physiology, Wayne State University School of Medicine, 4116 Scott Hall, 540 East Canfield Ave, 48201, Detroit, MI, USA aut NATIONALLICENCE 700 1- Jamison Jill Department of Physiology, Wayne State University School of Medicine, 4116 Scott Hall, 540 East Canfield Ave, 48201, Detroit, MI, USA aut NATIONALLICENCE 700 1- DeGracia Donald Department of Physiology, Wayne State University School of Medicine, 4116 Scott Hall, 540 East Canfield Ave, 48201, Detroit, MI, USA aut NATIONALLICENCE 773 0- Translational Stroke Research Springer US; http://www.springer-ny.com 4/6(2013-12-01), 589-603 1868-4483 4:6<589 2013 4 12975 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer