IGF-1 protects cardiac myocytes from hyperosmotic stress-induced apoptosis via CREB
| Autor: | Andres Collao, Guillermo Díaz-Araya, Carola Maldonado, Tatiana Adasme, Paola Cea, Sergio Lavandero, Mario Chiong |
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| Rok vydání: | 2005 |
| Předmět: |
MAPK/ERK pathway
Biophysics MAP Kinase Kinase 1 Apoptosis CREB Biochemistry p38 Mitogen-Activated Protein Kinases Rats Sprague-Dawley Phosphatidylinositol 3-Kinases Osmotic Pressure Ca2+/calmodulin-dependent protein kinase Myocyte Animals Myocytes Cardiac Calcium Signaling Insulin-Like Growth Factor I Phosphorylation Cyclic AMP Response Element-Binding Protein Molecular Biology Transcription factor Cells Cultured Cell Nucleus biology Chemistry Calcineurin Cell Biology Molecular biology Rats Protein Transport Calcium-Calmodulin-Dependent Protein Kinases biology.protein Intracellular Signal Transduction |
| Zdroj: | Biochemical and biophysical research communications. 336(4) |
| ISSN: | 0006-291X |
| Popis: | Hyperosmotic stress stimulates a rapid and pronounced apoptosis in cardiac myocytes which is attenuated by insulin-like growth factor-1 (IGF-1). Because in these cells IGF-1 induces intracellular Ca2+ increase, we assessed whether the cyclic AMP response element-binding protein (CREB) is activated by IGF-1 through Ca2+-dependent signalling pathways. In cultured cardiac myocytes, IGF-1 induced phosphorylation (6.5 ± 1.0-fold at 5 min), nuclear translocation (30 min post-stimulus) and DNA binding activity of CREB. IGF-1-induced CREB phosphorylation was mediated by MEK1/ERK, PI3-K, p38-MAPK, as well as Ca2+/calmodulin kinase and calcineurin. Exposure of cardiac myocytes to hyperosmotic stress (sorbitol 600 mOsm) decreased IGF-1-induced CREB activation Moreover, overexpression of a dominant negative CREB abolished the anti-apoptotic effects of IGF-1. Our results suggest that IGF-1 activates CREB through a complex signalling pathway, and this transcription factor plays an important role in the anti-apoptotic action of IGF-1 in cultured cardiac myocytes. |
| Databáze: | OpenAIRE |
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