Document Detail

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...
24285917 - Icat: development of an internet-based data collection method for ecological momentary ...
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:
  • Articles


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...