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Insulin-like growth factor-I prevents caspase-mediated apoptosis in Schwann cells
Authors
Altman
Altman
+44 more
Angevine
Artavanis-Tsakonas
Ase
Bascó
Bayer
Bovolenta
Brandt
Dahl
Das
de la Pompa
del Amo
Eckenhoff
Eddleston
Egan
Fujita
Gallahan
Gould
Hamada
Hatten
Higuchi
Hirano
Kimble
Kopan
Lardelli
Lardelli
Lardelli
Lindsell
Nagy
Nye
Pixley
Rakic
Reaume
Rebay
Rickmann
Ridet
Schnitzer
Shiga
Uyttendaele
Wang
Weinmaster
Weinmaster
Weinmaster
Wilkinson
Yuasa
Publication date
1 January 1999
Publisher
'Wiley'
Doi
Abstract
Both neurons and glia succumb to programmed cell death (PCD) when deprived of growth factors at critical periods in development or following injury. Insulin-like growth factor-I (IGF-I) prevents apoptosis in neurons in vitro. To investigate whether IGF-I can protect Schwann cells (SC) from apoptosis, SC were harvested from postnatal day 3 rats and maintained in serum-containing media until confluency. When cells were switched to serum-free defined media (DM) for 12–72 h, they underwent PCD. Addition of insulin or IGF-I prevented apoptosis. Bisbenzamide staining revealed nuclear condensation and formation of apoptotic bodies in SC grown in DM alone, but SC grown in DM plus IGF-I had normal nuclear morphology. The phosphatidylinositol 3-kinase (PI 3-K) inhibitor LY294002 blocked IGF-I–mediated protection. Caspase-3 activity was rapidly activated upon serum withdrawal in SC, and the caspase inhibitor BAF blocked apoptosis. These results suggest that IGF-I rescues SC from apoptosis via PI 3-K signaling which is upstream from caspase activation. © 1999 John Wiley & Sons, Inc. J Neurobiol 41: 540–548, 1999Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/34481/1/9_ftp.pd
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