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Expression of anti-aging type-XVII collagen (COL17A1/BP180) in hair follicle-associated pluripotent (HAP) stem cells during differentiation

  1. Author:
    Shirai, Kyoumi
    Obara, Koya
    Tohgi, Natsuko
    Yamazaki, Aiko
    Aki, Ryoichi
    Hamada, Yuko
    Arakawa, Nobuko
    Singh,Shree Ram
    Hoffman, Robert M.
    Amoh, Yasuyuki

  2. Author Address

    Kitasato Univ, Dept Dermatol, Sch Med, Sagamihara, Kanagawa, Japan.NCI, Basic Res Lab, Frederic, MD 21702 USA.AntiCanc Inc, San Diego, CA 92111 USA.Univ Calif San Diego, Dept Surg, San Diego, CA 92103 USA.
    1. Year: 2019
    2. Date: AUG
  2. Journal: TISSUE & CELL
  3. CHURCHILL LIVINGSTONE,
    1. 59
    2. Pages: 33-38
  5. Type of Article: Article
  6. ISSN: 0040-8166
  1. Abstract:

    Hair-follicle-associated pluripotent (HAP) stem cells reside in the upper part of the bulge area of the the hair follicle. HAP stem cells are nestin-positive and keratin 15-negative and have the capacity to differentiate into various types of cells in vitro. HAP stem cells are also involved in nerve and spinal cord regeneration in mouse models. Recently, it was shown that the DNA-damage response in non-HAP hair follicle stem cells induces proteolysis of type-XVII collagen (COL17A1/BP180), which is involved in hair-follicle stem-cell maintenance. COL17A1 proteolysis stimulated hair-follicle stem-cell aging, characterized by the loss of stemness signatures and hair-follicle miniaturization associated with androgenic alopecia. In the present study, we demonstrate that HAP stem cells co-express nestin and COL17A1 in vitro and in vivo. The expression of HAP stem cell markers (nestin and SSEA1) increased after HAP stem-cell colonies were formed, then decreased after differentiation to epidermal keratinocytes. In contrast COL17A1 increased after differentiation to epidermal keratinocytes. These results suggest that COL17A1 is important in differentiation of HAP stem cells.

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External Sources

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  2. DOI: 10.1016/j.tice.2019.06.001
  3. View record in Web of Science®
  4. WOS: 000478567400004

Library Notes

  1. Fiscal Year: FY2018-2019
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