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GRP78 induction by cyclosporin A in human HeLa cells
L Paslaru1, M Pinto, M Morange
1Unité de Génétique moléculaire, Ecole Normale Supérieure, Paris, France.
FEBS Letters
|August 22, 1994
Summary
Cyclosporin A (CsA), an immunosuppressive drug, triggers the production of stress protein GRP78 in HeLa cells at low doses. This CsA-induced GRP78 may explain some of CsA's physiological effects.
Area of Science:
- Cell Biology
- Molecular Biology
- Pharmacology
Background:
- Immunosuppressive drugs like cyclosporin A (CsA) and FK506 exhibit diverse cellular effects.
- Understanding the specific molecular mechanisms of these drugs is crucial for their therapeutic applications.
Purpose of the Study:
- To investigate the impact of CsA and FK506 on cellular stress responses.
- To identify specific proteins whose synthesis is modulated by these immunosuppressants.
Main Methods:
- Treatment of HeLa cells with varying concentrations of CsA and FK506.
- Analysis of protein synthesis, including stress proteins like GRP78 and heat shock proteins.
- Application of heat shock to induce cellular stress during drug treatment.
Main Results:
- Low concentrations of CsA induced the synthesis of GRP78, an endoplasmic reticulum stress protein.
- High concentrations of CsA resulted in a general reduction of protein synthesis.
- Heat shock during CsA treatment enhanced the synthesis of heat shock proteins.
- FK506 showed no significant effects on protein synthesis at any tested concentration.
Conclusions:
- Cyclosporin A, but not FK506, specifically induces GRP78 synthesis in HeLa cells.
- The overexpression of GRP78 may contribute to the observed physiological effects of CsA.
- The precise mechanism by which CsA induces GRP78 requires further investigation.