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Insulin‐like growth factor I rescues SH‐SY5Y human neuroblastoma cells from hyperosmotic induced programmed cell death
Author(s) -
Matthews Christopher C.,
Feldman Eva L.
Publication year - 1996
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199602)166:2<323::aid-jcp10>3.0.co;2-c
Subject(s) - sh sy5y , programmed cell death , viability assay , microbiology and biotechnology , apoptosis , cell culture , biology , cell growth , growth factor , insulin like growth factor , neuroblastoma , receptor , biochemistry , genetics
Abstract Insulin‐like growth factor I (IGF‐I) and the type I IGF receptor are widely distributed in developing and adult mammalian nervous systems. In vitro, IGF‐I is a mitogen for primary neurons and also for cells from the SH‐SY5Y human neuroblastoma cell line, a well‐characterized model system of neuronal growth. In the current study, we examined the effects of osmotic stress on SH‐SY5Y cell viability and the mechanism by which IGF‐I serves as a neuronal osmoprotectant. Within 24 hr, exposure of SH‐SY5Y cells to hyperosmotic serum‐free media decreased (1) the number of viable cells, (2) the rate of 3 H‐thymidine incorporation, and (3) cell cycle progression. The inclusion of 10 nM IGF‐I with hyperosmotic media prevented the loss of cell viability. The osmoprotective effects of IGF‐I were inhibited by α‐IR J , a blocking antibody of the type I IGF receptor. The observed loss of SH‐SY5Y cell viability following hyperosmotic shock was due to an induction of programmed cell death as determined by flow cytometry and gel electrophoresis. Our results suggest that IGF‐I can protect SH‐SY5Y cells from hyperosmotic induced programmed cell death. © 1996 Wiley‐Liss, Inc.