Dlk1 regulates quiescence in calcitonin receptor-mutant muscle stem cells.
Animals
Calcium-Binding Proteins
/ metabolism
Cell Differentiation
/ physiology
Cell Division
/ physiology
Cell Proliferation
/ physiology
Mice, Inbred C57BL
Mice, Transgenic
Muscle, Skeletal
/ metabolism
Receptors, Calcitonin
/ metabolism
Satellite Cells, Skeletal Muscle
/ metabolism
Stem Cells
/ metabolism
CalcR-PKA-Yap1 axis
Dlk1
calcitonin receptor
muscle stem cells
quiescence
Journal
Stem cells (Dayton, Ohio)
ISSN: 1549-4918
Titre abrégé: Stem Cells
Pays: England
ID NLM: 9304532
Informations de publication
Date de publication:
03 2021
03 2021
Historique:
received:
18
08
2020
accepted:
20
11
2020
pubmed:
10
12
2020
medline:
15
12
2021
entrez:
9
12
2020
Statut:
ppublish
Résumé
Muscle stem cells, also called muscle satellite cells (MuSCs), are responsible for skeletal muscle regeneration and are sustained in an undifferentiated and quiescent state under steady conditions. The calcitonin receptor (CalcR)-protein kinase A (PKA)-Yes-associated protein 1 (Yap1) axis is one pathway that maintains quiescence in MuSCs. Although CalcR signaling in MuSCs has been identified, the critical CalcR signaling targets are incompletely understood. Here, we show the relevance between the ectopic expression of delta-like non-canonical Notch ligand 1 (Dlk1) and the impaired quiescent state in CalcR-conditional knockout (cKO) MuSCs. Dlk1 expression was rarely detected in both quiescent and proliferating MuSCs in control mice, whereas Dlk1 expression was remarkably increased in CalcR-cKO MuSCs at both the mRNA and protein levels. It is noteworthy that all Ki67
Substances chimiques
Calcium-Binding Proteins
0
Dlk1 protein, mouse
0
Receptors, Calcitonin
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
306-317Informations de copyright
©AlphaMed Press 2020.
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