Autocrine regulation of mesenchymal progenitor cell fates orchestrates tooth eruption.
Animals
Autocrine Communication
/ physiology
Cell Differentiation
/ physiology
Dental Sac
/ cytology
Humans
Mesenchymal Stem Cells
/ cytology
Mice
Mice, Transgenic
Parathyroid Hormone-Related Protein
/ genetics
Receptor, Parathyroid Hormone, Type 1
/ genetics
Signal Transduction
/ physiology
Tooth Eruption
/ physiology
dental follicle
in vivo lineage-tracing experiment
mesenchymal progenitor cells
parathyroid hormone-related peptide
tooth eruption
Journal
Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876
Informations de publication
Date de publication:
08 01 2019
08 01 2019
Historique:
pubmed:
5
12
2018
medline:
13
3
2019
entrez:
5
12
2018
Statut:
ppublish
Résumé
Formation of functional skeletal tissues requires highly organized steps of mesenchymal progenitor cell differentiation. The dental follicle (DF) surrounding the developing tooth harbors mesenchymal progenitor cells for various differentiated cells constituting the tooth root-bone interface and coordinates tooth eruption in a manner dependent on signaling by parathyroid hormone-related peptide (PTHrP) and the PTH/PTHrP receptor (PPR). However, the identity of mesenchymal progenitor cells in the DF and how they are regulated by PTHrP-PPR signaling remain unknown. Here, we show that the PTHrP-PPR autocrine signal maintains physiological cell fates of DF mesenchymal progenitor cells to establish the functional periodontal attachment apparatus and orchestrates tooth eruption. A single-cell RNA-seq analysis revealed cellular heterogeneity of PTHrP
Identifiants
pubmed: 30509999
pii: 1810200115
doi: 10.1073/pnas.1810200115
pmc: PMC6329940
doi:
Substances chimiques
Parathyroid Hormone-Related Protein
0
Receptor, Parathyroid Hormone, Type 1
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
575-580Subventions
Organisme : NIDCR NIH HHS
ID : R01 DE024450
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE026666
Pays : United States
Organisme : NIDCR NIH HHS
ID : R03 DE027421
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2019 the Author(s). Published by PNAS.
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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