This work is dedicated to Professor H. G. Klingenberg.
Induction of heat shock proteins in short-term cultured hepatocytes derived from normal and chronically griseofulvin-treated mice†
Article first published online: 6 DEC 2005
Copyright © 1988 American Association for the Study of Liver Diseases
Volume 8, Issue 3, pages 607–612, May/June 1988
How to Cite
Zatloukal, K., Sohar, R., Lackinger, E. and Denk, H. (1988), Induction of heat shock proteins in short-term cultured hepatocytes derived from normal and chronically griseofulvin-treated mice. Hepatology, 8: 607–612. doi: 10.1002/hep.1840080328
- Issue published online: 6 DEC 2005
- Article first published online: 6 DEC 2005
- Manuscript Accepted: 6 OCT 1987
- Manuscript Received: 20 NOV 1986
- Fonds zur Förderung der wissenschaftlichen Forschung. Grant Numbers: P 4708, P 5803
Freshly isolated mouse hepatocytes were tested with respect to the induction of heat shock (stress) proteins by elevated temperature, sodium arsenite and ethanol treatment. With heat, arsenite and ethanol treatments, the synthesis of a protein with a molecular weight of 68 kD (heat shock protein 68) was predominantly elevated; arsenite and ethanol exerted their effects on heat shock protein synthesis in a dose-dependent manner. Hepatocytes derived from livers of chronically griseofulvin-pretreated mice differed in their response from normal hepatocytes in that ethanol was ineffective in these cells. These results indicate that different modes and pathways of the stress response exist, depending on the nature of the inducing agent but also on pretreatment conditions. In vivo, pathologic alterations of cells and organs (e.g., in the course of chronic diseases) can, therefore, be expected to modulate the stress response.