Hypothermia preserves expression of beta-actin mRNA in ischemic brain.
The expression of a cytoskeletal protein, beta-actin, mRNA was examined in hypothermic ischemic brains. Mongolian gerbils were subjected to forebrain ischemia by bilateral carotid occlusion of 10 min at 30 degrees C followed by normothermic reperfusion for 1 h or 6 h, 1 day or 3 days, 2 weeks or 1 month. The expression of beta-actin mRNA was determined in hypothermic controls and postischemic (PI) animals subjected to intra-ischemic hypothermia using in situ hybridization. On comparing the pattern of expression of beta-actin in hypothermic ischemic brains with that in normothermic ischemic brains, it was noted that there was no significant decline in its expression in the CA1 region of hypothermic ischemic brains as noted in the normothermic ischemic brains (reported by us previously). Only one hypothermic ischemic animal in the 2 week PI period showed marked reduction in its expression in the CA1 region. These results indicate that hypothermia leads to preservation of the expression of a cytoskeletal protein, beta-actin, in a selectively vulnerable region of the brain following ischemia.
Wu
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Department of Pathology, Michigan State University, East Lansing 48824, USA.
Evans
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Kumar
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D000199:Actins / Q000235:genetics*; D000704:Analysis of Variance; D000818:Animals; D001483:Base Sequence; D005849:Gerbillinae; D007036:Hypothermia, Induced; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D008297:Male; D008969:Molecular Sequence Data; D009419:Nerve Tissue Proteins / Q000235:genetics*; D012333:RNA, Messenger / Q000096:biosynthesis*
D000199:Actins; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger