Deficiency of Crif1 in hair follicle stem cells retards hair growth cycle in adult mice.
Animals
Cell Cycle Proteins
/ metabolism
Cell Differentiation
/ physiology
Epidermis
/ growth & development
Hair
/ growth & development
Hair Follicle
/ growth & development
Mice
Mice, Knockout
Mitochondria
/ metabolism
Mitochondrial Proteins
/ metabolism
Oxidative Phosphorylation
Peptides
/ metabolism
Stem Cells
/ metabolism
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2020
2020
Historique:
received:
15
08
2019
accepted:
09
04
2020
entrez:
25
4
2020
pubmed:
25
4
2020
medline:
24
7
2020
Statut:
epublish
Résumé
Hair growth is the cyclically regulated process that is characterized by growing phase (anagen), regression phase (catagen) and resting phase (telogen). Hair follicle stem cells (HFSCs) play pivotal role in the control of hair growth cycle. It has been notified that stem cells have the distinguished metabolic signature compared to differentiated cells, such as the preference to glycolysis rather than mitochondrial respiration. Crif1 is a mitochondrial protein that regulates the synthesis and insertion of oxidative phosphorylation (OXPHOS) polypeptides to inner membrane of mitochondria. Several studies demonstrate that tissue-specific knockout of Crif1 leads to mitochondrial dysfunction. In this study, we investigated the effect of mitochondrial dysfunction in terms of Crif1 deficiency on the hair growth cycle of adult mice. We created two kinds of inducible conditional knockout (icKO) mice. In epidermal specific icKO mice (Crif1 K14icKO), hair growth cycle was significantly retarded compared to wild type mice. Similarly, HFSC specific icKO mice (Crif1 K15icKO) showed significant retardation of hair growth cycle in depilation-induced anagen model. Interestingly, flow cytometry revealed that HFSC populations were maintained in Crif1 K15icKO mice. These results suggest that mitochondrial function in HFSCs is important for the progression of hair growth cycle, but not for maintenance of HFSCs.
Identifiants
pubmed: 32330194
doi: 10.1371/journal.pone.0232206
pii: PONE-D-19-23115
pmc: PMC7182249
doi:
Substances chimiques
Cell Cycle Proteins
0
Crif1 protein, mouse
0
Mitochondrial Proteins
0
Peptides
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0232206Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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