Topical Estrogen Accelerates Hair Regrowth in Mice after Chemotherapy-Induced Alopecia by Favoring the Dystrophic Catagen Response Pathway to Damage

Ulrich Ohnemus, Murat Ünalan, Bori Handjiski, Ralf Paus

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

Estrogen receptor ligands are important modulators of skin physiology and are involved in the control of normal hair follicle cycling. Here, we have studied the effects of topically applied 17-β-estradiol on pathologic hair follicle cycling as seen during chemotherapy-induced alopecia, one of the major unresolved problems of clinical oncology. For this study we employed a well-established murine model that mimics chemotherapy-induced alopecia in humans. For precisely quantifying the area of hair loss and hair regrowth in this model in vivo, we developed a simple planimetric assay (dotmatrix planimetry). We show that topical 17-β-estradiol significantly alters the cycling response of murine follicles to cyclophosphamide, whereas the estrogen antagonist ICI 182.780 exerted no such effects. Initially, topical 17-β-estradiol enhanced chemotherapy-induced alopecia significantly by forcing the follicles into the dystrophic catagen response pathway to hair follicle damage, whereas follicles treated by ICI 182.780 or vehicle shifted into the dystrophic anagen response pathway. Consequently, the regrowth of normally pigmented hair shafts after chemotherapy-induced alopecia was significantly accelerated in the 17-β-estradiol treated group. Our data encourage one to explore topical estrogens as a potential stimulant for hair re-growth after chemotherapy-induced alopecia.

Original languageEnglish (US)
Pages (from-to)7-13
Number of pages7
JournalJournal of Investigative Dermatology
Volume122
Issue number1
DOIs
StatePublished - Jan 1 2004
Externally publishedYes

Fingerprint

Chemotherapy
Alopecia
Hair
Estrogens
Estradiol
Drug Therapy
Hair Follicle
Estrogen Antagonists
Skin Physiological Phenomena
Oncology
Physiology
Medical Oncology
Estrogen Receptors
Cyclophosphamide
Modulators
Assays
Skin
Ligands
Growth

Keywords

  • Cyclophosphamide
  • Dotmatrix planimetry
  • Hair follicle dystrophy
  • Hair loss
  • ICI 182.780

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology
  • Cell Biology

Cite this

Topical Estrogen Accelerates Hair Regrowth in Mice after Chemotherapy-Induced Alopecia by Favoring the Dystrophic Catagen Response Pathway to Damage. / Ohnemus, Ulrich; Ünalan, Murat; Handjiski, Bori; Paus, Ralf.

In: Journal of Investigative Dermatology, Vol. 122, No. 1, 01.01.2004, p. 7-13.

Research output: Contribution to journalArticle

@article{2d3cae3ca53a4c2e92fe648aea65be03,
title = "Topical Estrogen Accelerates Hair Regrowth in Mice after Chemotherapy-Induced Alopecia by Favoring the Dystrophic Catagen Response Pathway to Damage",
abstract = "Estrogen receptor ligands are important modulators of skin physiology and are involved in the control of normal hair follicle cycling. Here, we have studied the effects of topically applied 17-β-estradiol on pathologic hair follicle cycling as seen during chemotherapy-induced alopecia, one of the major unresolved problems of clinical oncology. For this study we employed a well-established murine model that mimics chemotherapy-induced alopecia in humans. For precisely quantifying the area of hair loss and hair regrowth in this model in vivo, we developed a simple planimetric assay (dotmatrix planimetry). We show that topical 17-β-estradiol significantly alters the cycling response of murine follicles to cyclophosphamide, whereas the estrogen antagonist ICI 182.780 exerted no such effects. Initially, topical 17-β-estradiol enhanced chemotherapy-induced alopecia significantly by forcing the follicles into the dystrophic catagen response pathway to hair follicle damage, whereas follicles treated by ICI 182.780 or vehicle shifted into the dystrophic anagen response pathway. Consequently, the regrowth of normally pigmented hair shafts after chemotherapy-induced alopecia was significantly accelerated in the 17-β-estradiol treated group. Our data encourage one to explore topical estrogens as a potential stimulant for hair re-growth after chemotherapy-induced alopecia.",
keywords = "Cyclophosphamide, Dotmatrix planimetry, Hair follicle dystrophy, Hair loss, ICI 182.780",
author = "Ulrich Ohnemus and Murat {\"U}nalan and Bori Handjiski and Ralf Paus",
year = "2004",
month = "1",
day = "1",
doi = "10.1046/j.0022-202X.2003.22120.x",
language = "English (US)",
volume = "122",
pages = "7--13",
journal = "Journal of Investigative Dermatology",
issn = "0022-202X",
publisher = "Nature Publishing Group",
number = "1",

}

TY - JOUR

T1 - Topical Estrogen Accelerates Hair Regrowth in Mice after Chemotherapy-Induced Alopecia by Favoring the Dystrophic Catagen Response Pathway to Damage

AU - Ohnemus, Ulrich

AU - Ünalan, Murat

AU - Handjiski, Bori

AU - Paus, Ralf

PY - 2004/1/1

Y1 - 2004/1/1

N2 - Estrogen receptor ligands are important modulators of skin physiology and are involved in the control of normal hair follicle cycling. Here, we have studied the effects of topically applied 17-β-estradiol on pathologic hair follicle cycling as seen during chemotherapy-induced alopecia, one of the major unresolved problems of clinical oncology. For this study we employed a well-established murine model that mimics chemotherapy-induced alopecia in humans. For precisely quantifying the area of hair loss and hair regrowth in this model in vivo, we developed a simple planimetric assay (dotmatrix planimetry). We show that topical 17-β-estradiol significantly alters the cycling response of murine follicles to cyclophosphamide, whereas the estrogen antagonist ICI 182.780 exerted no such effects. Initially, topical 17-β-estradiol enhanced chemotherapy-induced alopecia significantly by forcing the follicles into the dystrophic catagen response pathway to hair follicle damage, whereas follicles treated by ICI 182.780 or vehicle shifted into the dystrophic anagen response pathway. Consequently, the regrowth of normally pigmented hair shafts after chemotherapy-induced alopecia was significantly accelerated in the 17-β-estradiol treated group. Our data encourage one to explore topical estrogens as a potential stimulant for hair re-growth after chemotherapy-induced alopecia.

AB - Estrogen receptor ligands are important modulators of skin physiology and are involved in the control of normal hair follicle cycling. Here, we have studied the effects of topically applied 17-β-estradiol on pathologic hair follicle cycling as seen during chemotherapy-induced alopecia, one of the major unresolved problems of clinical oncology. For this study we employed a well-established murine model that mimics chemotherapy-induced alopecia in humans. For precisely quantifying the area of hair loss and hair regrowth in this model in vivo, we developed a simple planimetric assay (dotmatrix planimetry). We show that topical 17-β-estradiol significantly alters the cycling response of murine follicles to cyclophosphamide, whereas the estrogen antagonist ICI 182.780 exerted no such effects. Initially, topical 17-β-estradiol enhanced chemotherapy-induced alopecia significantly by forcing the follicles into the dystrophic catagen response pathway to hair follicle damage, whereas follicles treated by ICI 182.780 or vehicle shifted into the dystrophic anagen response pathway. Consequently, the regrowth of normally pigmented hair shafts after chemotherapy-induced alopecia was significantly accelerated in the 17-β-estradiol treated group. Our data encourage one to explore topical estrogens as a potential stimulant for hair re-growth after chemotherapy-induced alopecia.

KW - Cyclophosphamide

KW - Dotmatrix planimetry

KW - Hair follicle dystrophy

KW - Hair loss

KW - ICI 182.780

UR - http://www.scopus.com/inward/record.url?scp=1642534522&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=1642534522&partnerID=8YFLogxK

U2 - 10.1046/j.0022-202X.2003.22120.x

DO - 10.1046/j.0022-202X.2003.22120.x

M3 - Article

C2 - 14962083

AN - SCOPUS:1642534522

VL - 122

SP - 7

EP - 13

JO - Journal of Investigative Dermatology

JF - Journal of Investigative Dermatology

SN - 0022-202X

IS - 1

ER -