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A Role for Ethanol-Induced Oxidative Stress in Controlling Lineage Commitment of Mesenchymal Stromal Cells Through Inhibition of Wnt/β-Catenin Signaling

Thyroid Hormone-Mediated Growth and Differentiation of Growth Plate Chondrocytes Involves IGF-1 Modulation of β-Catenin Signaling

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Thyroid Hormone-Mediated Growth and Differentiation of Growth Plate Chondrocytes Involves IGF-1 Modulation of β-Catenin Signaling

Content Provider	PubMed Central
Author	Wang, Lai Shao, Yvonne Y. Tracy, Ballock R.
Copyright Year	2010
Abstract	Thyroid hormone regulates terminal differentiation of growth plate chondrocytes in part through modulation of the Wnt/β-catenin signaling pathway. Insulin-like growth factor 1 (IGF-1) has been described as a stabilizer of β-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/β-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 β-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. T3 activates IGF-1/IGF1R signaling and IGF-1-dependent PI3K/Akt/GSK-3β signaling in growth plate chondrocytes undergoing proliferation and differentiation to prehypertrophy. T3-mediated Wnt-4 expression, β-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 β-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/GSK3β pathway, cell hypertrophy is likely due to activation of Wnt/β-catenin signaling, which is at least in part initiated by IGF-1 signaling or the IGF-1-activated PI3K/Akt signaling pathway. © 2010 American Society for Bone and Mineral Research.
Related Links	http://dx.doi.org/10.1002/jbmr.5
Ending Page	1146
Page Count	9
Starting Page	1138
File Format	PDF
ISSN	08840431
e-ISSN	15234681
Journal	Journal of Bone and Mineral Research
Issue Number	5
Volume Number	25
Language	English
Publisher	Wiley Subscription Services, Inc., A Wiley Company
Publisher Date	2010-05-01
Access Restriction	Open
Rights Holder	Wiley Subscription Services, Inc., A Wiley Company
Subject Keyword	Endocrinology, Diabetes and Metabolism Orthopedics and Sports Medicine Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Orthopedics and Sports Medicine Endocrinology, Diabetes and Metabolism

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