Stress proteins and reperfusion stress in the liver.
Blood reperfusion after temporary liver ischemia induces the expression of heat shock genes and the synthesis of heat shock proteins (hsps), in particular hsp 70. Induction requires a certain duration of ischemia, suggesting that cell damage before reperfusion is essential for activation of heat shock genes. The expression of the hsp 70 gene is preceded by activation of the cellular protooncogenes c-fos and c-jun. However, the product of these genes, which is transcription factor AP-1, seems unnecessary for activation of the hsp 70 gene, which does not require the integrity of protein synthesis. Hsp genes seem to behave as "early response genes," enabling the cell to respond to emergency situations.
Bernelli-Zazzera
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A
Istituto di Patologia Generale dell'Università, Milan, Italy.
Cairo
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G
Schiaffonati
L
L
Tacchini
L
L
D000818:Animals; D015180:Electrophoresis, Gel, Two-Dimensional; D015870:Gene Expression; D006360:Heat-Shock Proteins / Q000378:metabolism*; D007511:Ischemia / Q000378:metabolism; D008099:Liver / Q000098:blood supply / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D015427:Reperfusion Injury / Q000378:metabolism*
D006360:Heat-Shock Proteins; D012333:RNA, Messenger