Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2003-11-24
pubmed:abstractText
Chondrocyte differentiation is a fundamental process during endochondral ossification. Several factors regulate maturation via the activity of downstream signaling pathways that target specific transcription factors and regulate chondrocyte-specific genes. In this study, we investigated the mechanisms involved in the regulation of chick lower sternal chondrocyte maturation upon stimulation by retinoic acid (RA) and the bone morphogenetic protein BMP2. RA-induced Runx2 in lower sternal chondrocyte cultures and over-expression of wild-type (WT) Runx2 enhanced colX and alkaline phosphatase activity, while over-expression of dominant negative Runx2 was inhibitory. Furthermore, WT Runx2 enhanced the effects of both BMP2 and RA on colX expression, while the effects of both growth factors were completely blocked in cultures over-expressing dominant negative Runx2. Similarly, WT Runx2 enhanced the induction of colX by Smad1. Smad1 and Runx2 were found to act cooperatively at the chicken type X collagen promoter and elimination of either the putative Smad binding site or Runx2 binding site eliminated responsiveness to BMP2, RA, or either of the transcription factors. Altogether the results show cross talk between the BMP-associated Smads and Runx2 during chondrocyte differentiation and dependence upon both signals for induction of the type X collagen promoter. Factors or signals that alter either of these transcription factors regulate the rate of chondrocyte differentiation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Bone Morphogenetic Protein 2, http://linkedlifedata.com/resource/pubmed/chemical/Bone Morphogenetic Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Collagen Type X, http://linkedlifedata.com/resource/pubmed/chemical/Core Binding Factor Alpha 1 Subunit, http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Neoplasm Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Smad Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators, http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors, http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta, http://linkedlifedata.com/resource/pubmed/chemical/Tretinoin
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0730-2312
pubmed:author
pubmed:copyrightInfo
Copyright 2003 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
90
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1287-98
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:14635200-Animals, pubmed-meshheading:14635200-Bone Morphogenetic Protein 2, pubmed-meshheading:14635200-Bone Morphogenetic Proteins, pubmed-meshheading:14635200-Cell Differentiation, pubmed-meshheading:14635200-Cells, Cultured, pubmed-meshheading:14635200-Chick Embryo, pubmed-meshheading:14635200-Chondrocytes, pubmed-meshheading:14635200-Collagen Type X, pubmed-meshheading:14635200-Core Binding Factor Alpha 1 Subunit, pubmed-meshheading:14635200-DNA-Binding Proteins, pubmed-meshheading:14635200-Gene Expression Regulation, Developmental, pubmed-meshheading:14635200-Neoplasm Proteins, pubmed-meshheading:14635200-Promoter Regions, Genetic, pubmed-meshheading:14635200-Signal Transduction, pubmed-meshheading:14635200-Smad Proteins, pubmed-meshheading:14635200-Trans-Activators, pubmed-meshheading:14635200-Transcription Factors, pubmed-meshheading:14635200-Transforming Growth Factor beta, pubmed-meshheading:14635200-Tretinoin
pubmed:year
2003
pubmed:articleTitle
Runx2/Cbfa1 stimulation by retinoic acid is potentiated by BMP2 signaling through interaction with Smad1 on the collagen X promoter in chondrocytes.
pubmed:affiliation
The Center for Musculoskeletal Research, University of Rochester, Rochester, New York 14642, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.