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Insulin-like growth factor-I prevents caspase-mediated apoptosis in Schwann cells.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Delaney, C. L. |
| Copyright Year | 1999 |
| 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. |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://deepblue.lib.umich.edu/bitstream/handle/2027.42/34481/9_ftp.pdf;sequence=1 |
| Alternate Webpage(s) | https://deepblue.lib.umich.edu/bitstream/handle/2027.42/34481/9_ftp.pdf?isAllowed=y&sequence=1 |
| Alternate Webpage(s) | https://deepblue.lib.umich.edu/bitstream/handle/2027.42/34481/9_ftp.pdf?sequence=1 |
| PubMed reference number | 10590177v1 |
| Volume Number | 41 |
| Issue Number | 4 |
| Journal | Journal of neurobiology |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | 1-Phosphatidylinositol 3-Kinase Apoptosis Apoptotic Bodies Baker's Antifol Caspase Inhibitors Cell Death Growth Factor LY 294002 Neuroglia Otitis Media Schwann Cells Signal Transduction Somatomedins |
| Content Type | Text |
| Resource Type | Article |
