Insulin-like growth factor I is the key growth factor in serum that protects neuroblastoma cells from hyperosmotic-induced apoptosis
dc.contributor.author | Van Golen, Cynthia M. | en_US |
dc.contributor.author | Feldman, Eva L. | en_US |
dc.date.accessioned | 2006-04-19T13:34:33Z | |
dc.date.available | 2006-04-19T13:34:33Z | |
dc.date.issued | 2000-01 | en_US |
dc.identifier.citation | Van Golen, Cynthia M.; Feldman, Eva L. (2000)."Insulin-like growth factor I is the key growth factor in serum that protects neuroblastoma cells from hyperosmotic-induced apoptosis." Journal of Cellular Physiology 182(1): 24-32. <http://hdl.handle.net/2027.42/34442> | en_US |
dc.identifier.issn | 0021-9541 | en_US |
dc.identifier.issn | 1097-4652 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/34442 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=10567913&dopt=citation | en_US |
dc.description.abstract | Neuroblastoma is a childhood tumor of the peripheral nervous system that remains largely uncurable by conventional methods. Mannitol induces apoptosis in neuroblastoma cell types and insulin-like growth factor I (IGF-I) protects these cells from hyperosmotic-induced apoptosis by affecting apoptosis-regulatory proteins. In the current study, we investigate factors that enable SH-SY5Y neuroblastoma cells to survive in the presence of an apoptotic stimulus. When SH-SY5Y cells are exposed to high mannitol concentrations, more than 60% of the cells are apoptotic within 48 h. Normal CS prevents hyperosmotic-induced apoptosis in a dose-dependent manner, with 0.6% CS protecting 50% of the cells, and 3% CS rescuing more than 70% of the cells from apoptosis. Serum also delays the commitment point for SH-SY5Y cells from 9 h to 35 h. A survey of several growth factors, including epidermal growth factor (EGF), platelet-derived growth factor (PDGF), nerve growth factor (NGF), fibroblast growth factor (FGF), and IGF-I reveals that IGF-I is a component of serum necessary for protection of neuroblastoma cells from death. Mitochondrial membrane depolarization occurs in greater than 40% of the cells after mannitol exposure and caspase-3 activation is increased in high mannitol conditions after 9 h. IGF-I blocks both the mitochondrial membrane depolarization and caspase-3 activation normally induced by hyperosmotic treatment in neuroblastoma cells. Our results suggest that (1) IGF-I is a key factor in serum necessary for protection from death and (2) IGF-I acts upstream from the mitochondria and the caspases to prevent apoptosis in human neuroblastoma. J. Cell. Physiol. 182:24–32, 2000. © 2000 Wiley-Liss, Inc. | en_US |
dc.format.extent | 256605 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | John Wiley & Sons, Inc. | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Cell & Developmental Biology | en_US |
dc.title | Insulin-like growth factor I is the key growth factor in serum that protects neuroblastoma cells from hyperosmotic-induced apoptosis | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbsecondlevel | Kinesiology and Sports | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Neurology and Neuroscience Program, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Neurology and Neuroscience Program, University of Michigan, Ann Arbor, Michigan ; University of Michigan Department of Neurology, 200 Zina Pitcher Place, 4414 Kresge III, Ann Arbor, MI 48109 | en_US |
dc.identifier.pmid | 10567913 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/34442/1/3_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/(SICI)1097-4652(200001)182:1<24::AID-JCP3>3.0.CO;2-6 | en_US |
dc.identifier.source | Journal of Cellular Physiology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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