Wnt Signaling Regulates Pulp Volume and Dentin Thickness

ABSTRACT Odontoblasts, cementoblasts, ameloblasts, and osteoblasts all form mineralized tissues in the craniofacial complex, and all these cell types exhibit active Wnt signaling during postnatal life. We set out to understand the functions of this Wnt signaling, by evaluating the phenotypes of mice...

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Veröffentlicht in:Journal of bone and mineral research 2014-04, Vol.29 (4), p.892-901
Hauptverfasser: Lim, Won Hee, Liu, Bo, Cheng, Du, Hunter, Daniel J, Zhong, Zhendong, Ramos, Daniel M, Williams, Bart O, Sharpe, Paul T, Bardet, Claire, Mah, Su‐jung, Helms, Jill A
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container_end_page 901
container_issue 4
container_start_page 892
container_title Journal of bone and mineral research
container_volume 29
creator Lim, Won Hee
Liu, Bo
Cheng, Du
Hunter, Daniel J
Zhong, Zhendong
Ramos, Daniel M
Williams, Bart O
Sharpe, Paul T
Bardet, Claire
Mah, Su‐jung
Helms, Jill A
description ABSTRACT Odontoblasts, cementoblasts, ameloblasts, and osteoblasts all form mineralized tissues in the craniofacial complex, and all these cell types exhibit active Wnt signaling during postnatal life. We set out to understand the functions of this Wnt signaling, by evaluating the phenotypes of mice in which the essential Wnt chaperone protein, Wntless was eliminated. The deletion of Wls was restricted to cells expressing Osteocalcin (OCN), which in addition to osteoblasts includes odontoblasts, cementoblasts, and ameloblasts. Dentin, cementum, enamel, and bone all formed in OCN‐Cre;Wlsfl/fl mice but their homeostasis was dramatically affected. The most notable feature was a significant increase in dentin volume and density. We attribute this gain in dentin volume to a Wnt‐mediated misregulation of Runx2. Normally, Wnt signaling stimulates Runx2, which in turn inhibits dentin sialoprotein (DSP); this inhibition must be relieved for odontoblasts to differentiate. In OCN‐Cre;Wlsfl/fl mice, Wnt pathway activation is reduced and Runx2 levels decline. The Runx2‐mediated repression of DSP is relieved and odontoblast differentiation is accordingly enhanced. This study demonstrates the importance of Wnt signaling in the homeostasis of mineralized tissues of the craniofacial complex. © 2014 American Society for Bone and Mineral Research.
doi_str_mv 10.1002/jbmr.2088
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We set out to understand the functions of this Wnt signaling, by evaluating the phenotypes of mice in which the essential Wnt chaperone protein, Wntless was eliminated. The deletion of Wls was restricted to cells expressing Osteocalcin (OCN), which in addition to osteoblasts includes odontoblasts, cementoblasts, and ameloblasts. Dentin, cementum, enamel, and bone all formed in OCN‐Cre;Wlsfl/fl mice but their homeostasis was dramatically affected. The most notable feature was a significant increase in dentin volume and density. We attribute this gain in dentin volume to a Wnt‐mediated misregulation of Runx2. Normally, Wnt signaling stimulates Runx2, which in turn inhibits dentin sialoprotein (DSP); this inhibition must be relieved for odontoblasts to differentiate. In OCN‐Cre;Wlsfl/fl mice, Wnt pathway activation is reduced and Runx2 levels decline. The Runx2‐mediated repression of DSP is relieved and odontoblast differentiation is accordingly enhanced. 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source MEDLINE; Access via Wiley Online Library; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals
subjects Animals
Core Binding Factor Alpha 1 Subunit - genetics
Dental Pulp - anatomy & histology
DENTIN
Dentin - anatomy & histology
Mice
ODONTOBLAST
PULP
Real-Time Polymerase Chain Reaction
Signal Transduction
Wnt Proteins - metabolism
WNT SIGNALING PATHWAY
title Wnt Signaling Regulates Pulp Volume and Dentin Thickness
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