Regulation of Schwann cell nerve growth factor receptor by cyclic adenosine 3′,5′‐monophosphate

Abstract

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 mRNA in sequence and size. The amount of this NGF mRNA was lower in cAMP analogue-treated than in untreated Schwann cells.

Neuronal modulation of schwann cell glial fibrillary acidic protein (GFAP)

“…1988; Mokuno et al, 1988;Lemke and Chao, 1988), it is reasonable to hypothesize that axonal contact, by elevating Schwann cell CAMP, induces the transcription of genes (Roesler et al, 1988) that participate in Schwann cell differentiation. However, the contrasting effects on Schwann cell phentoype of contact with large axons (induction of the synthesis of Po and other myelin proteins, but not of GFAP) and with small axons (induction of the synthesis of GFAP, but not of the myelin proteins) strongly support the concept that unidentified axonal trophic signals, in addition to those modulating Schwann cell CAMP content, must participate in the neuronal regulation of Schwann cell phenotype.…”

The nerve growth factor receptor: a multicomponent system that mediates the actions of the neurotrophin family of proteins

“…Testosterone reduces p75 NGF receptor mRNA levels within Sertoli cells [104]. Within Schwann cells, levels of p75 receptor protein are reduced by forskolin and cyclic AMP analogues [123] and increased by exposure to isolated axonal components [124].…”

Axon‐Schwann cell interactions regulate the expression of fibroblast growth factor‐5 (FGF‐5)

“…The effects of forskolin on cultured Schwann cells complement these findings. Forskolin activates adenylate cyclase (Seamon et al, 1981), and mimics many of the effects of axon-Schwann cell interactions, such as the upregulation of myelin-related lipids and proteins (Sobue and Pleasure, 1984;Lemke and Chao, 1988;Morgan et al, 1991;Bharucha et al, 1993), and the downregulation of p75LNTR (Mokuno et al, 1988;Morgan et al, 1991). Thus, Schwann cell expression of FGF-5 mRNA, like that of p75LNTR, is induced by Wallerian degeneration and inhibited by elevating intracellular cyclic AMP.…”