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
Insulin-like growth factor-I prevents apoptosis in neurons after nerve growth factor withdrawal
β Scribed by Russell, James W. ;Windebank, Anthony J. ;Schenone, Angelo ;Feldman, Eva L.
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 273 KB
- Volume
- 36
- Category
- Article
- ISSN
- 0022-3034
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β¦ Synopsis
Insulin-like growth factor-I (IGF-NGF withdrawal. The antiapoptotic effect of IGF-I I) is emerging as an important growth factor able to was completely blocked by LY294002, an inhibitor of modulate the programmed cell death (PCD) pathway mediated by the cysteine-dependent aspartate prote-PI 3-kinase signaling, but not by the mitogen-activated ases (caspases); however, little is known about the protein (MAP) kinase/extracellular signal-regulated effect of IGF-I after nerve growth factor (NGF) withprotein kinase (ERK) activated protein kinase inhibidrawal in neurons. To begin to understand the neutor PD98059. Functional IGF-I receptors were extenronal death-sparing effect of IGF-I under NGF-free sively expressed both in rat and human DRG neurons, conditions, we tested whether embryonic sensory doralthough they were most abundant in the neuronal sal root ganglion neurons (DRG) were able to survive growth cone. Collectively, these findings indicate that in defined serum-free medium in the presence of IGF-IGF-I, signaling though the PI-3 kinase pathway, is I. We further studied the role of IGF-I signaling and important in modulating PCD in cultured DRG neucaspase inhibition after NGF withdrawal. NGF withrons after NGF withdrawal, and IGF-I may be imdrawal produced histological changes of apoptosis inportant in DRG embryogenesis. α§ 1998 John Wiley & cluding chromatin condensation, shrinkage of the per-
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