Incubation of C6 glioma cells in the presence of aminoglutethimide, an inhibitor of cholesterol metabolism, together with either adenosine 3',5'-cyclic monophosphate (CAMP) analogues or agents that increase CAMP synthesis, such as cholera toxin, forskolin, and isoproterenol, stimulated the rate of p
Regulation of Schwann cell nerve growth factor receptor by cyclic adenosine 3′,5′-monophosphate
✍ Scribed by K. Mokuno; G. Sobue; U. R. Reddy; J. Wurzer; B. Kreider; H. Hotta; P. Baron; A. H. Ross; Dr. D. Pleasure
- Publisher
- John Wiley and Sons
- Year
- 1988
- Tongue
- English
- Weight
- 893 KB
- Volume
- 21
- Category
- Article
- ISSN
- 0360-4012
No coin nor oath required. For personal study only.
✦ Synopsis
Previous studies indicated that Schwann cells in immature nerves express nerve growth factor (NGF) receptors, and that this expression is down regulated during development but re-induced by Wallerian degeneration. It was also shown that immature Schwann cells are induced to express galactocerebroside and other molecules characteristic of mature Schwann cells by either contact with an axon or treatment with the cyclic adenosine 3 ',5'-monophosphate (CAMP) analogues dibutyryl cAMP (dbcAMP) and 8-bromo CAMP or the adenylate cyclase activator forskolin. In the present study, NGF receptors on the surface of cultured Schwann cells were demonstrated by binding of an anti-rat NGF receptor monoclonal antibody or of radioiodinated NGF. Treatment of cultured Schwann cells with cAMP analogues or forskolin resulted in a progressive decrease in both immunoreactive NGF receptors and radioiodinated NGF binding. The cultured Schwann cells contained a polyadenylated RNA species homologous with human melanoma NGF receptor mRVA in sequence and size. The amount of this NGF mRNA was lower in CAMP analogue-treated than in untreated Schwann cells.
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