Linked Life Data

12168799

Source:http://linkedlifedata.com/resource/pubmed/id/12168799

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2002-8-9
pubmed:abstractText
The formation of cranial bone requires the differentiation of osteoblasts from undifferentiated mesenchymal cells. The balance between osteoblast recruitment, proliferation, differentiation and apoptosis in sutures between cranial bones is essential for calvarial bone formation. The mechanisms that control human osteoblasts during normal calvarial bone formation and premature suture ossification (craniosynostosis) begin to be understood. Our studies of the human calvaria osteoblast phenotype and calvarial bone formation showed that premature fusion of the sutures in non-syndromic and syndromic (Apert syndrome) craniosynostoses results from precocious osteoblast differentiation. We showed that Fibroblast Growth Factor-2 (FGF-2), FGF receptor-2 (FGFR-2) and Bone Morphogenetic Protein-2 (BMP-2), three essential factors involved in skeletal development, regulate the proliferation, differentiation and apoptosis in human calvaria osteoblasts. Mechanisms that induce the differentiated osteoblast phenotype have also been identified in human calvaria osteoblasts. We demonstrated the implication of molecules (N-cadherin, Il-1) and signaling pathways (src, PKC) by which these local factors modulate human calvaria osteoblast differentiation and apoptosis. The identification of these essential signaling molecules provides new insights into the pathways controlling the differentiated osteoblast phenotype, and leads to a more comprehensive view in the mechanisms that control normal and premature cranial ossification in humans.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0213-3911
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
877-85
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:12168799-Apoptosis, pubmed-meshheading:12168799-Bone Morphogenetic Protein 2, pubmed-meshheading:12168799-Bone Morphogenetic Proteins, pubmed-meshheading:12168799-Cell Differentiation, pubmed-meshheading:12168799-Cell Division, pubmed-meshheading:12168799-Fibroblast Growth Factor 2, pubmed-meshheading:12168799-Gene Expression Regulation, pubmed-meshheading:12168799-Humans, pubmed-meshheading:12168799-Models, Biological, pubmed-meshheading:12168799-Osteoblasts, pubmed-meshheading:12168799-Phenotype, pubmed-meshheading:12168799-Receptor, Fibroblast Growth Factor, Type 2, pubmed-meshheading:12168799-Receptor Protein-Tyrosine Kinases, pubmed-meshheading:12168799-Receptors, Fibroblast Growth Factor, pubmed-meshheading:12168799-Signal Transduction, pubmed-meshheading:12168799-Skull, pubmed-meshheading:12168799-Time Factors, pubmed-meshheading:12168799-Transforming Growth Factor beta
pubmed:year
2002
pubmed:articleTitle
Regulation of human cranial osteoblast phenotype by FGF-2, FGFR-2 and BMP-2 signaling.
pubmed:affiliation
INSERM U349, Hopital Lariboisière, Paris, France. pierre.marie@inserm.lrb.ap-hop-paris.fr
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't