Hair follicle stem cells provide a functional niche for melanocyte stem cells

Tanimura, Shintaro, Tadokoro, Yuko, Inomata. Ken, Binh, Nguyen Thanh, Nishie, Wataru, Yamazaki, Satoshi, Nakauchi, Hiromitsu, Tanaka, Yoshio, McMillan, James R., Sawamura, Daisuke, Yancey, Kim, Shimizu, Hiroshi and Nishimura, Emi K. (2011) Hair follicle stem cells provide a functional niche for melanocyte stem cells. Cell Stem Cell, 82 2: 177-187. doi:10.1016/j.stem.2010.11.029

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Author Tanimura, Shintaro
Tadokoro, Yuko
Inomata. Ken
Binh, Nguyen Thanh
Nishie, Wataru
Yamazaki, Satoshi
Nakauchi, Hiromitsu
Tanaka, Yoshio
McMillan, James R.
Sawamura, Daisuke
Yancey, Kim
Shimizu, Hiroshi
Nishimura, Emi K.
Title Hair follicle stem cells provide a functional niche for melanocyte stem cells
Journal name Cell Stem Cell   Check publisher's open access policy
ISSN 1934-5909
Publication date 2011-02-04
Sub-type Article (original research)
DOI 10.1016/j.stem.2010.11.029
Volume 82
Issue 2
Start page 177
End page 187
Total pages 11
Place of publication Cambridge, MA, U.S.A.
Publisher Elsevier, Cell Press
Language eng
Abstract In most previous termstem cellnext term systems, the organization of the previous termstem cell nichenext term and the anchoring matrix required for previous termstem cellnext term maintenance are largely unknown. We report here that collagen XVII (COL17A1/BP180/BPAG2), previous termanext term hemidesmosomal transmembrane collagen, is highly expressed in previous termhair follicle stem cellsnext term (HFSCs) and is required for the maintenance not only of HFSCs but also of previous termmelanocyte stem cellsnext term (MSCs), which do not express Col17a1 but directly adhere to HFSCs. Mice lacking Col17a1 show premature previous termhairnext term graying and previous termhairnext term loss. Analysis of Col17a1-null mice revealed that COL17A1 is critical for the self-renewal of HFSCs through maintaining their quiescence and immaturity, potentially explaining the mechanism underlying previous termhairnext term loss in human COL17A1 deficiency. Moreover, forced expression of COL17A1 in basal keratinocytes, including HFSCs, in Col17a1-null mice rescues MSCs from premature differentiation and restores TGF-β signaling, demonstrating that HFSCs function as previous termanext term critical regulatory component of the MSC previous termniche.next term
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status Non-UQ
Additional Notes Available online 3 February, 2011.

Document type: Journal Article
Sub-type: Article (original research)
Collections: Non HERDC
School of Medicine Publications
 
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Created: Fri, 18 Feb 2011, 20:40:08 EST by Dr James Mcmillan on behalf of School of Medicine