Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2009-6-3
pubmed:abstractText
Transforming growth factor-beta (TGF-beta) signaling exerts a wide spectrum of biological functions. To investigate TGF-beta signaling in amelogenesis, we initially assessed the expression of TGF-beta1 and TGF-beta receptor 1 (TGFBR1) in developing teeth by immunohistochemistry. Both TGF-beta1 and TGFBR1 were strongly expressed in secreting ameloblasts. Next, we studied the effects of TGF-beta signaling on the expression of MMP20 and KLK4 mRNA using ameloblast-lineage cells (ALC) in vitro. Our RT-PCR study showed that TGF-beta1, TGFBR1, and enamel matrix proteases (MMP20 and KLK4) were expressed in ALC. Following TGF-beta1 treatment, the expression of MMP20 mRNA, but not KLK4 mRNA, was significantly upregulated. To further confirm the TGF-beta signaling involvement in the MMP20 expression, we constructed the activated TGFBR1 vector and transfected the construct into ALC. The activated TGFBR1 notably promoted MMP20 expression, but had no obvious effects on the KLK4 mRNA expression. Our studies strongly suggest that TGF-beta signaling involved in amelogenesis is partially mediated by regulating the expression of MMP20 mRNA.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1932-8494
pubmed:author
pubmed:copyrightInfo
(c) 2009 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:volume
292
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
885-90
pubmed:dateRevised
2009-12-16
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
TGF-beta1 and TGFBR1 are expressed in ameloblasts and promote MMP20 expression.
pubmed:affiliation
Department of Pediatric and Preventive Dentistry, Institute of Stomatology, Weifang Medical University, Weifang City, Shandong Province, People's Republic of China. yuguanggao@wfmc.edu.cn
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't