| Transforming growth factor-beta 1 regulates axon/Schwann cell interactions. | |
| | |
| Jump to Full Text | |
MedLine Citation:
|
PMID: 7536747 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
We have investigated the potential regulatory role of TGF-beta in the interactions of neurons and Schwann cells using an in vitro myelinating system. Purified populations of neurons and Schwann cells, grown alone or in coculture, secrete readily detectable levels of the three mammalian isoforms of TGF-beta; in each case, virtually all of the TGF-beta activity detected is latent. Expression of TGF-beta 1, a major isoform produced by Schwann cells, is specifically and significantly downregulated as a result of axon/Schwann cell interactions. Treatment of Schwann cells or Schwann cell/neuron cocultures with TGF-beta 1, in turn, has dramatic effects on proliferation and differentiation. In the case of purified Schwann cells, treatment with TGF-beta 1 increases their proliferation, and it promotes a pre- or nonmyelinating Schwann cell phenotype characterized by increased NCAM expression, decreased NGF receptor expression, inhibition of the forskolin-mediated induction of the myelin protein P0, and induction of the Schwann cell transcription factor suppressed cAMP-inducible POU protein. Addition of TGF-beta 1 to the cocultures inhibits many of the effects of the axon on Schwann cells, antagonizing the proliferation induced by contact with neurons, and, strikingly, blocking myelination. Ultrastructural analysis of the treated cultures confirmed the complete inhibition of myelination and revealed only rudimentary ensheathment of axons. Associated defects of the Schwann cell basal lamina and reduced expression of laminin were also detected. These effects of TGF-beta 1 on Schwann cell differentiation are likely to be direct effects on the Schwann cells themselves which express high levels of TGF-beta 1 receptors when cocultured with neurons. The regulated expression of TGF-beta 1 and its effects on Schwann cells suggest that it may be an important autocrine and paracrine mediator of neuron/Schwann cell interactions. During development, TGF-beta 1 could serve as an inhibitor of Schwann cell proliferation and myelination, whereas after peripheral nerve injury, it may promote the transition of Schwann cells to a proliferating, nonmyelinating phenotype, and thereby enhance the regenerative response. |
| | |
Authors:
|
S Einheber; M J Hannocks; C N Metz; D B Rifkin; J L Salzer |
Related Documents
:
|
21661347 - The influence of the different morphological changes on gastric mucosa on somatostatin ... 16181067 - Molecular targets to promote central nervous system regeneration. 1878937 - Dissociation of photoreceptor cells from the pineal organ of the lamprey, lampetra japo... 15068007 - Fibrin/schwann cell matrix in poly-epsilon-caprolactone conduits enhances guided nerve ... 15181167 - Expression of the sodium-myo-inositol cotransporter smit2 at the apical membrane of mad... 21264367 - Saponins from plumeria acuminata ait induce cell growth inhibition and apoptosis of ora... |
Publication Detail:
|
Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
|
Title: The Journal of cell biology Volume: 129 ISSN: 0021-9525 ISO Abbreviation: J. Cell Biol. Publication Date: 1995 Apr |
Date Detail:
|
Created Date: 1995-05-22 Completed Date: 1995-05-22 Revised Date: 2010-09-13 |
Medline Journal Info:
|
Nlm Unique ID: 0375356 Medline TA: J Cell Biol Country: UNITED STATES |
Other Details:
|
Languages: eng Pagination: 443-58 Citation Subset: IM |
Affiliation:
|
Department of Cell Biology, New York University Medical School, New York 10016, USA. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Animals Axons / drug effects, physiology* Basement Membrane / drug effects, ultrastructure Cell Adhesion Molecules, Neuronal / biosynthesis Cell Communication / drug effects* Cell Division / drug effects Forskolin / pharmacology Ganglia, Spinal / cytology, embryology Laminin / biosynthesis Myelin P0 Protein Myelin Proteins / biosynthesis Nerve Fibers, Myelinated / physiology, ultrastructure Nerve Tissue Proteins / biosynthesis Neurons / cytology, metabolism, physiology Octamer Transcription Factor-6 Rats Receptors, Nerve Growth Factor / biosynthesis Schwann Cells / cytology*, drug effects, physiology, ultrastructure Transcription Factors / biosynthesis Transforming Growth Factor beta / analysis, pharmacology, physiology* |
| Grant Support | |
ID/Acronym/Agency:
|
CA 09161/CA/NCI NIH HHS; CA 23753/CA/NCI NIH HHS; NS 26001/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
|
0/Cell Adhesion Molecules, Neuronal; 0/Laminin; 0/Myelin P0 Protein; 0/Myelin Proteins; 0/Nerve Tissue Proteins; 0/Pou3f1 protein, rat; 0/Receptors, Nerve Growth Factor; 0/Transcription Factors; 0/Transforming Growth Factor beta; 132052-52-9/Octamer Transcription Factor-6; 66428-89-5/Forskolin |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
| Full Text | |
|
Journal Information Journal ID (nlm-ta): J Cell Biol ISSN: 0021-9525 ISSN: 1540-8140 Publisher: The Rockefeller University Press |
Article Information Download PDF  Print publication date: Day: 2 Month: 4 Year: 1995 Volume: 129 Issue: 2 First Page: 443 Last Page: 458 ID: 2199906 Publisher Id: 95238541 PubMed Id: 7536747 |
| Transforming growth factor-beta 1 regulates axon/Schwann cell interactions | |
Article Categories:
|
|
Previous Document: Transcription-dependent redistribution of the large subunit of RNA polymerase II to discrete nuclear...
Next Document: Plasticity in epithelial cell phenotype: modulation by expression of different cadherin cell adhesio...