Linked Life Data

9618141

Source:http://linkedlifedata.com/resource/pubmed/id/9618141

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-7-1
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0021-9541
pubmed:author
pubmed:issnType
Print
pubmed:volume
176
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
22-31
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:9618141-Adenovirus E1A Proteins, pubmed-meshheading:9618141-Animals, pubmed-meshheading:9618141-Cell Communication, pubmed-meshheading:9618141-Cell Count, pubmed-meshheading:9618141-Cell Differentiation, pubmed-meshheading:9618141-Cell Line, pubmed-meshheading:9618141-Down-Regulation, pubmed-meshheading:9618141-Fibroblast Growth Factor 2, pubmed-meshheading:9618141-Gene Expression Regulation, Developmental, pubmed-meshheading:9618141-Immunohistochemistry, pubmed-meshheading:9618141-Mice, pubmed-meshheading:9618141-Muscle Development, pubmed-meshheading:9618141-Nerve Growth Factors, pubmed-meshheading:9618141-Polymerase Chain Reaction, pubmed-meshheading:9618141-Rats, pubmed-meshheading:9618141-Receptor, Fibroblast Growth Factor, Type 2, pubmed-meshheading:9618141-Receptor Protein-Tyrosine Kinases, pubmed-meshheading:9618141-Receptors, Fibroblast Growth Factor, pubmed-meshheading:9618141-Receptors, Nerve Growth Factor, pubmed-meshheading:9618141-Signal Transduction, pubmed-meshheading:9618141-Up-Regulation
pubmed:year
1998
pubmed:articleTitle
Regulation of nerve growth factor and its low-affinity receptor (p75NTR) during myogenic differentiation.
pubmed:affiliation
Department of Cell and Molecular Biology, Institute for Biochemistry and Biotechnology, University of Braunschweig, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't