ArticleThe Journal of investigative dermatology2015
Testing chemotherapeutic agents in the feather follicle identifies a selective blockade of cell proliferation and a key role for sonic hedgehog signaling in chemotherapy-induced tissue damage.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 29 citations in OpenAlex.
- Genetic dissection of leg and back feather follicle density in yellow-feathered broiler: integrative GWAS and transcriptome analysis reveal the regulatory role of SERPINF1.Poultry science · 2026Article
- Down-regulation of Shh in the hair follicles of mice during chemotherapy-induced hair loss is mediated by the JAK/STAT1 signaling pathway.FEBS open bio · 2026Article
- Stingless bee propolis promotes hair follicle regeneration and melanocyte function in chemotherapy-induced alopecia mouse model.Experimental animals · 2026Article
- Convergence of external and internal stressors on a stress-responsive enhancer of theProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Establishment of a culture model for the prolonged maintenance of chicken feather follicles structure in vitro.PloS one · 2022Article
- The global regulatory logic of organ regeneration: circuitry lessons from skin and its appendages.Biological reviews of the Cambridge Philosophical Society · 2021Article
- Cooling-mediated protection from chemotherapy drug-induced cytotoxicity in human keratinocytes by inhibition of cellular drug uptake.PloS one · 2020Article
- Priming mobilization of hair follicle stem cells triggers permanent loss of regeneration after alkylating chemotherapy.Nature communications · 2019Article
- Genetic analysis of a novel antioxidant multi-target iron chelator, M30 protecting against chemotherapy-induced alopecia in mice.BMC cancer · 2019Article
- Chemotherapy-Induced Hair Loss: The Use of Biomarkers for Predicting Alopecic Severity and Treatment Efficacy.Biomarker insights · 2019Article
- Contraction of basal filopodia controls periodic feather branching via Notch and FGF signaling.Nature communications · 2018Article
- A Clinical and Biological Guide for Understanding Chemotherapy-Induced Alopecia and Its Prevention.The oncologist · 2018Review
- Mobilizing Transit-Amplifying Cell-Derived Ectopic Progenitors Prevents Hair Loss from Chemotherapy or Radiation Therapy.Cancer research · 2017Article
- Cellular Senescence as the Causal Nexus of Aging.Frontiers in genetics · 2016Review
- Feather on the Cap of Medicine.The Journal of investigative dermatology · 2015Article
- Drug discovery for alopecia: gone today, hair tomorrow.Expert opinion on drug discovery · 2015Review
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8 authors at 3 institutions in 3 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Chemotherapeutic agents induce complex tissue responses in vivo and damage normal organ functions. Here we use the feather follicle to investigate details of this damage response. We show that cyclophosphamide treatment, which causes chemotherapy-induced alopecia in mice and man, induces distinct defects in feather formation: feather branching is transiently and reversibly disrupted, thus leaving a morphological record of the impact of chemotherapeutic agents, whereas the rachis (feather axis) remains unperturbed. Similar defects are observed in feathers treated with 5-fluorouracil or taxol but not with doxorubicin or arabinofuranosyl cytidine (Ara-C). Selective blockade of cell proliferation was seen in the feather branching area, along with a downregulation of sonic hedgehog (Shh) transcription, but not in the equally proliferative rachis. Local delivery of the Shh inhibitor, cyclopamine, or Shh silencing both recapitulated this effect. In mouse hair follicles, those chemotherapeutic agents that disrupted feather formation also downregulated Shh gene expression and induced hair loss, whereas doxorubicin or Ara-C did not. Our results reveal a mechanism through which chemotherapeutic agents damage rapidly proliferating epithelial tissue, namely via the cell population-specific, Shh-dependent inhibition of proliferation. This mechanism may be targeted by future strategies to manage chemotherapy-induced tissue damage.
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