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  3. Hair follicle transit amplifying cells phagocytose dead cells after radiotherapeutic and chemotherapeutic injuries for timely regeneration

Hair follicle transit amplifying cells phagocytose dead cells after radiotherapeutic and chemotherapeutic injuries for timely regeneration

  • J Invest Dermatol. 2023 Aug 18;S0022-202X(23)02493-4. doi: 10.1016/j.jid.2023.07.012.
Jin-Bon Hong 1,  Wei-Hung Wang 2,  Yao-Wen Hsu 2,  Suet Yee Tee 2,  Yueh-Feng Wu 2,  Wen-Yen Huang 2,  Shih-Fan Lai 3,  Sung-Jan Lin 4
Affiliations

Affiliations

  • 1 Department of Dermatology, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan.
  • 2 Department of Biomedical Engineering, College of Medicine and College of Engineering, National Taiwan University, Taipei, Taiwan.
  • 3 Department of Biomedical Engineering, College of Medicine and College of Engineering, National Taiwan University, Taipei, Taiwan; Division of Radiation Oncology, Department of Oncology, National Taiwan University Hospital, Taipei, Taiwan.
  • 4 Department of Dermatology, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan; Department of Biomedical Engineering, College of Medicine and College of Engineering, National Taiwan University, Taipei, Taiwan; Research Center for Developmental Biology and Regenerative Medicine, National Taiwan University, Taipei, Taiwan; Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan. Electronic address: drsjlin@ntu.edu.tw.
PMID: 37598868 DOI: 10.1016/j.jid.2023.07.012
Abstract

Efficient clearance of dead cells is critical for tissue regeneration following injuries. How dead cells are removed from the skin after radiotherapy and chemotherapy is unclear. Herein, we found that radiotherapeutic and chemotherapeutic damage induced extensive Apoptosis of highly proliferative transit-amplifying cells (TACs) in hair follicles. These apoptotic cells disappeared rapidly in the early stage of regenerative attempts, and the lost structures were regenerated with transient and low-level inflammation. Without the recruitment of macrophages as scavengers, the dying cells were engulfed directly by adjacent surviving TACs, which produced mature phagosomes through fusion with lysosomes in a manner similar to professional phagocytosis and remained active in proliferation. Autophagy did not contribute significantly to the clearance of engulfed cell debris. Perturbing phagocytosis in the TACs hindered apoptotic cell removal, delayed structural recovery, and aggravated hair loss. Therefore, TACs are capacitated with both proliferative and efferocytic functions that facilitate tissue regeneration after tissue injury.

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