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  3. Medical Genomics and Proteomics / 基因體暨蛋白體醫學研究所
  4. Mobilizing transit-amplifying cell-derived ectopic progenitors prevents hair loss from chemotherapy or radiation therapy
 
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Mobilizing transit-amplifying cell-derived ectopic progenitors prevents hair loss from chemotherapy or radiation therapy

Journal
Cancer Research
Journal Volume
77
Journal Issue
22
Pages
6083-6096
Date Issued
2017
Author(s)
Huang W.-Y.
SHIH-FAN LAI  
HSIEN-YI CHIU  
Chang M.
Plikus M.V.
CHIH-CHIEH CHAN  
YOU-TZUNG CHEN  
PO-NIEN TSAO  
TSUNG-LIN YANG  
Lee, Hsuan-Shu  
Chi P.  
SUNG-JAN LIN  
DOI
10.1158/0008-5472.CAN-17-0667
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85033789603&doi=10.1158%2f0008-5472.CAN-17-0667&partnerID=40&md5=d7d602454c1c89d16b26f2ebf3828f0a
https://scholars.lib.ntu.edu.tw/handle/123456789/520417
Abstract
Genotoxicity-induced hair loss from chemotherapy and radiotherapy is often encountered in cancer treatment, and there is a lack of effective treatment. In growing hair follicles (HF), quiescent stem cells (SC) are maintained in the bulge region, and hair bulbs at the base contain rapidly dividing, yet genotoxicity-sensitive transit-amplifying cells (TAC) that maintain hair growth. How genotoxicity-induced HF injury is repaired remains unclear. We report here that HFs mobilize ectopic progenitors from distinct TAC compartments for regeneration in adaptation to the severity of dystrophy induced by ionizing radiation (IR). Specifically, after low-dose IR, keratin 5? basal hair bulb progenitors, rather than bulge SCs, were quickly activated to replenish matrix cells and regenerated all concentric layers of HFs, demonstrating their plasticity. After high-dose IR, when both matrix and hair bulb cells were depleted, the surviving outer root sheath cells rapidly acquired an SC-like state and fueled HF regeneration. Their progeny then homed back to SC niche and supported new cycles of HF growth. We also revealed that IR induced HF dystrophy and hair loss and suppressed WNT signaling in a p53- and dose-dependent manner. Augmenting WNT signaling attenuated the suppressive effect of p53 and enhanced ectopic progenitor proliferation after genotoxic injury, thereby preventing both IR- and cyclophosphamide-induced alopecia. Hence, targeted activation of TAC-derived progenitor cells, rather than quiescent bulge SCs, for anagen HF repair can be a potential approach to prevent hair loss from chemotherapy and radiotherapy. ?2017 AACR.
SDGs

[SDGs]SDG3

Other Subjects
keratin; protein p53; alkylating agent; cyclophosphamide; cytokeratin 5; alopecia; animal cell; animal experiment; animal model; animal tissue; Article; cancer chemotherapy; cancer radiotherapy; cell plasticity; cell proliferation; cell regeneration; controlled study; depletion; disease severity; dystrophy; extracellular matrix; female; genotoxicity; hair follicle cell; hair growth; hair loss; hair root; ionizing radiation; low energy radiation; mouse; nonhuman; priority journal; progeny; stem cell; stem cell niche; transit amplifying cell; Wnt signaling; alopecia; animal; C57BL mouse; cell proliferation; confocal microscopy; cytology; gene expression; genetics; hair follicle; knockout mouse; metabolism; pathophysiology; regeneration; stem cell; transgenic mouse; Alopecia; Animals; Antineoplastic Agents, Alkylating; Cell Proliferation; Cyclophosphamide; Female; Gene Expression; Hair Follicle; Keratin-5; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Microscopy, Confocal; Radiation, Ionizing; Regeneration; Stem Cells; Wnt Signaling Pathway
Publisher
American Association for Cancer Research Inc.
Type
journal article

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