Insulin-like growth factor-I is an osmoprotectant in human neuroblastoma cells
Section snippets
Materials
Tissue culture flasks and plates were purchased from Corning (Corning, NY, U.S.A.). Dulbecco's modified Eagle's medium (DMEM), Hank's balanced salt solution (HBSS) and calf serum (CS) were from Gibco BRL (Gaithersburg, MD, U.S.A.). IGF-I was stored in 10 mM acetic acid at −80°C. Solutions containing IGF-I were stored at 4°C and used within three days. RNase A, proteinase K, tosyl-l-chloromethylketone and tosyl-l-phenylmethylketone were from Boehringer Mannheim (Germany). [3H]Leucine (1 mCi/ml)
Appearance of cell nuclei after hyperosmotic exposure
The nuclei of cells undergoing programmed cell death often experience a progressive condensation that results in the splitting of the nucleus into individual membrane-bound spheres. Our previous results demonstrated that approximately 40% of unprotected cells become detached within the first 24 h of exposure to hyperosmotic medium.[21]To determine the temporal relationship between changes in nuclear morphology and the state of cell attachment we used the fluorescent DNA-binding dye bisbenzimide
Discussion
Plasma hyperosmolarity is a common systemic feature of diseases with serious neurological consequences.[60]We have previously reported that SH-SY5Y cells, a well-characterized model of human neuronal growth and differentation,37, 38, 64show arrested growth and die when exposed to media made hyperosmotic by the addition of glucose, NaCl or mannitol.[40]This in vitro paradigm of hyperosmolar-coupled neuronal dysfunction was used to screen for agents which could serve as neural osmoprotectants. In
Conclusions
In summary, IGF-I can protect SH-SY5Y cells from hyperosmotic-coupled programmed cell death. The neuroprotective effect of IGF-I was not due to the traditional mitogenic or growth-promoting activities of IGF-I[21]and did not appear to require active protein synthesis. Addition of IGF-I up to the point of commitment to death markedly increased neuronal survival, implying a rapid onset of IGF-I action. Inhibitors of proteolytic activity prevented neuronal DNA fragmentation, suggesting that IGF-I
Acknowledgements
This study was supported by R29NS32843 (ELF), NIH NINDS T32 NS07222 (CCM) and grants from the Juvenile Diabetes Foundation no. 194130 (ELF) and the American Diabetes Association (ELF). The authors wish to thank Dr Kelli Sullivan for expert editorial assistance, James Beals for figure preparation and Judith Boldt for manuscript preparation.
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