Document Detail


Regulation of nerve growth factor and its low-affinity receptor (p75NTR) during myogenic differentiation.
MedLine Citation:
PMID:  9618141     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In our preceding report, we have shown that nerve growth factor (NGF) and its low-affinity receptor (p75NTR) are expressed in C2C12 myoblasts and downregulated during myogenic differentiation. Furthermore, NGF affects myogenic differentiation and cell growth via p75NTR and downregulation of p75NTR is essential for myogenic differentiation (Seidl et al., 1998). Here we show that NGF and p75NTR are regulated by mechanisms preceding terminal differentiation in myogenic cells. These mechanisms include cell-density phenomena such as cell-cell contact as well as signaling of basic fibroblast growth factor (FGF-2) and its receptor (FGFR1). Downregulation of NGF and p75NTR occurred as a consequence of increasing cell density, an important trigger for the onset of myogenic differentiation. FGF-2 and FGFR1 were shown to be present in C2C12 cells and exogenous FGF-2 induced NGF and p75NTR expression, implying that FGF/FGFR signaling is an upstream regulator of the NGF/p75NTR system. The fact that FGF-2 could suspend yet not abolish density-induced downregulation indicates that cell-cell contact counteracts the FGF effect and ultimately terminates NGF/p75NTR signaling. This evidence, together with the observation that p75NTR expression is suppressed in muscle progenitors, which constitutively express adenovirus E1A proteins and thus lack the competence of myogenic differentiation, underline the important role for the NGF/p75NTR system in the interplay of multiple factors and biological systems that balance myogenic differentiation at the appropriate spatial and temporal level.
Authors:
C Erck; C Meisinger; C Grothe; K Seidl
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  176     ISSN:  0021-9541     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  1998 Jul 
Date Detail:
Created Date:  1998-07-01     Completed Date:  1998-07-01     Revised Date:  2012-06-05    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  22-31     Citation Subset:  IM    
Affiliation:
Department of Cell and Molecular Biology, Institute for Biochemistry and Biotechnology, University of Braunschweig, Germany.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adenovirus E1A Proteins / genetics
Animals
Cell Communication / physiology
Cell Count
Cell Differentiation / physiology*
Cell Line
Down-Regulation / physiology
Fibroblast Growth Factor 2 / metabolism
Gene Expression Regulation, Developmental / genetics*
Immunohistochemistry
Mice
Muscle Development*
Nerve Growth Factors / metabolism*
Polymerase Chain Reaction
Rats
Receptor Protein-Tyrosine Kinases / metabolism
Receptor, Fibroblast Growth Factor, Type 2
Receptors, Fibroblast Growth Factor / metabolism
Receptors, Nerve Growth Factor / metabolism*
Signal Transduction / physiology
Up-Regulation / physiology
Chemical
Reg. No./Substance:
0/Adenovirus E1A Proteins; 0/Nerve Growth Factors; 0/Receptors, Fibroblast Growth Factor; 0/Receptors, Nerve Growth Factor; 103107-01-3/Fibroblast Growth Factor 2; EC 2.7.10.1/Fgfr2 protein, mouse; EC 2.7.10.1/Fgfr2 protein, rat; EC 2.7.10.1/Receptor Protein-Tyrosine Kinases; EC 2.7.10.1/Receptor, Fibroblast Growth Factor, Type 2

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Evidence for the participation of nerve growth factor and its low-affinity receptor (p75NTR) in the ...
Next Document:  Effect of aging on EGF-stimulated replication of specific genes in rat hepatocytes.