Induction of Apg-1, a Member of the Heat Shock Protein 110 Family, Following Transient Forebrain Ischemia in the Rat Brain

• Published in: Biochemical and biophysical research communications Vol. 247; no. 3; pp. 796 - 801
• Main Authors: Xue, Jing-Hui, Fukuyama, Hidenao, Nonoguchi, Kohsuke, Kaneko, Yoshiyuki, Kido, Tsuneo, Fukumoto, Manabu, Fujibayashi, Yasuhisa, Itoh, Katsuhiko, Fujita, Jun
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 29.06.1998
• Subjects: Animals; Brain - metabolism; Brain Ischemia - physiopathology; Disease Models, Animal; Gene Expression Regulation - genetics; Heat-Shock Proteins - metabolism; HSP70 Heat-Shock Proteins; In Situ Hybridization; Male; Rats; Rats, Wistar; RNA, Messenger - metabolism; Temperature
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1006/bbrc.1998.8894

Apg-1(Osp94) and apg-2 belong to the heat shock protein (hsp)110 family. In mouse somatic cells the apg-1and hsp105/ 110transcripts are inducible by a 32°C to 39°C heat shock, while apg-2is not heat-inducible. Since ischemia is known to induce expression of hsp70, its effect on expression of apg-1was assessed by using the 20-min forebrain ischemia model of the rat. In the cerebral cortex, Northern blot analysis and in situ hybridization histochemistry demonstrated an increased expression in neuronal cells of apg-1transcripts 3 h after the onset of reperfusion, with a peak at 12 h, followed by a decline. In the hippocampus, the level was increased at 3 h, remained constant until 24 h, and then declined. Transcript levels of apg-2as well as hsp105were also increased under the present conditions, indicating that the expression of apg-2was differentially regulated in response to heat and ischemic stresses. The induction kinetics of hsp105, but neither apg-2nor hsp70, were identical to those of apg-1. These results demonstrated that brain ischemia/reperfusion induced expression of each member of the hsp110 family, although the regulatory mechanisms may not be the same. They also suggest a significant role of apg-1 in both the ischemic-and heat-stress responses and in the normal functioning of the non-stressed neuronal cells.