Linked Life Data

20200966

Source:http://linkedlifedata.com/resource/pubmed/id/20200966

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2010-5-24
pubmed:abstractText
Thyroid hormone regulates terminal differentiation of growth plate chondrocytes in part through modulation of the Wnt/beta-catenin signaling pathway. Insulin-like growth factor 1 (IGF-1) has been described as a stabilizer of beta-catenin, and thyroid hormone is a known stimulator of IGF-1 receptor expression. The purpose of this study was to test the hypothesis that IGF-1 signaling is involved in the interaction between the thyroid hormone and the Wnt/beta-catenin signaling pathways in regulating growth plate chondrocyte proliferation and differentiation. The results show that IGF-1 and the IGF- receptor (IGF1R) stimulate Wnt-4 expression and beta-catenin activation in growth plate chondrocytes. The positive effects of IGF-1/IGF1R on chondrocyte proliferation and terminal differentiation are partially inhibited by the Wnt antagonists sFRP3 and Dkk1. T(3) activates IGF-1/IGF1R signaling and IGF-1-dependent PI3K/Akt/GSK-3beta signaling in growth plate chondrocytes undergoing proliferation and differentiation to prehypertrophy. T(3)-mediated Wnt-4 expression, beta-catenin activation, cell proliferation, and terminal differentiation of growth plate chondrocytes are partially prevented by the IGF1R inhibitor picropodophyllin as well as by the PI3K/Akt signaling inhibitors LY294002 and Akti1/2. These data indicate that the interactions between thyroid hormone and beta-catenin signaling in regulating growth plate chondrocyte proliferation and terminal differentiation are modulated by IGF-1/IGF1R signaling through both the Wnt and PI3K/Akt signaling pathways. While chondrocyte proliferation may be triggered by the IGF-1/IGF1R-mediated PI3K/Akt/GSK3beta pathway, cell hypertrophy is likely due to activation of Wnt/beta-catenin signaling, which is at least in part initiated by IGF-1 signaling or the IGF-1-activated PI3K/Akt signaling pathway.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-10544181, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-10862751, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-11014246, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-11035789, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-12432069, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-12466191, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-12748651, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-12782654, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-14749359, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-15130559, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-15334055, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-15590974, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-15845624, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-16051666, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-16793760, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-16857753, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-17337262, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-17431620, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-17446238, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-17592018, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-17708712, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-17960591, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-18397998, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-18405384, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-8063865, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-8132746, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-8402901, http://linkedlifedata.com/resource/pubmed/commentcorrection/20200966-8402902
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1523-4681
pubmed:author
pubmed:copyrightInfo
(c) 2010 American Society for Bone and Mineral Research.
pubmed:issnType
Electronic
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1138-46
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:20200966-Animals, pubmed-meshheading:20200966-Cell Differentiation, pubmed-meshheading:20200966-Cell Proliferation, pubmed-meshheading:20200966-Cells, Cultured, pubmed-meshheading:20200966-Chondrocytes, pubmed-meshheading:20200966-Growth Plate, pubmed-meshheading:20200966-Insulin-Like Growth Factor I, pubmed-meshheading:20200966-Phosphatidylinositol 3-Kinases, pubmed-meshheading:20200966-Podophyllotoxin, pubmed-meshheading:20200966-Proto-Oncogene Proteins c-akt, pubmed-meshheading:20200966-Rats, pubmed-meshheading:20200966-Rats, Sprague-Dawley, pubmed-meshheading:20200966-Receptor, IGF Type 1, pubmed-meshheading:20200966-Signal Transduction, pubmed-meshheading:20200966-Triiodothyronine, pubmed-meshheading:20200966-Wnt Proteins, pubmed-meshheading:20200966-Wnt4 Protein, pubmed-meshheading:20200966-beta Catenin
pubmed:year
2010
pubmed:articleTitle
Thyroid hormone-mediated growth and differentiation of growth plate chondrocytes involves IGF-1 modulation of beta-catenin signaling.
pubmed:affiliation
Orthopaedic Research Center, Department of Orthopaedic Surgery, The Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural