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Deficiency of Crif1 in hair follicle stem cells retards hair growth cycle in adult mice.
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- Additional Information
- Source:
Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
- Publication Information:
Original Publication: San Francisco, CA : Public Library of Science
- Subject Terms:
- Abstract:
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.
Competing Interests: The authors have declared that no competing interests exist.
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- Accession Number:
0 (Cell Cycle Proteins)
0 (Crif1 protein, mouse)
0 (Mitochondrial Proteins)
0 (Peptides)
- Publication Date:
Date Created: 20200425 Date Completed: 20200723 Latest Revision: 20200723
- Publication Date:
20231215
- Accession Number:
PMC7182249
- Accession Number:
10.1371/journal.pone.0232206
- Accession Number:
32330194
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