The Hair Follicle: A Paradoxical Androgen Target Organ

  title={The Hair Follicle: A Paradoxical Androgen Target Organ},
  author={Valerie Anne Randall and Nigel A. Hibberts and M. Julie Thornton and K. Hamada and Alison E. Merrick and Shoji Kato and Terry Jenner and Isobel De Oliveira and Andrew G Messenger},
  journal={Hormone Research in Paediatrics},
  pages={243 - 250}
Androgens are the main regulator of normal human hair growth. After puberty, they promote transformation of vellus follicles, producing tiny, unpigmented hairs, to terminal ones, forming larger pigmented hairs, in many areas, e.g. the axilla. However, they have no apparent effect on the eyelashes, but can cause the opposite transformation on the scalp leading to the replacement of terminal hairs by vellus ones and the gradual onset of androgenetic alopecia. This paradox appears to be an unique… 

Figures from this paper

The involvement of androgens in human hair growth

Identifying key paracrine factors which may be involved in androgen regulated changes in the hair follicles could improve the understanding of the mechanism of androgen action in human hair follicle action.

Molecular Basis of Androgenetic Alopecia

This paradoxical difference underpins the successful transplant of unaffected follicles from non-balding regions into the androgen-sensitive, balding areas during corrective surgery for androgenetic alopecia.

Androgen actions on the human hair follicle: perspectives

This work has shown that androgens enhance inducible nitric oxide synthase from occipital DP cells and stem cell factor for positive regulation of hair growth in beard and negative regulation of balding DP cells, and involves crosstalk between androgen and Wnt/β‐catenin signalling.

The hair follicle as an estrogen target and source.

It is argued that the time has come to pay estrogen-mediated signaling the full attention it deserves in future endocrinological therapy of common hair growth disorders.

Androgen modulation of Wnt/β-catenin signaling in androgenetic alopecia

The androgen-induced dermal papilla secreted factors on stimulating catagen entry in hair follicles and the molecular cross-talk between AR and Wnt/β-catenin signaling with a brief mention on alternative treatment strategy targeting Wnt-catanin signaling for promoting hair growth are analysed.

The genetically programmed hair growth cycle and alopecia: what is there to know?

The last 20 years have seen a vast change in research activity into the regulation of hair growth in health and disease and, over the next 5 years, this should include further important glimpses of the nature of the hair follicle's clock machinery.

Differences in expression of specific biomarkers distinguish human beard from scalp dermal papilla cells.

C cultured dermal papilla cells provide a cell-based model system that is reflective of the biology of in vivo hair follicle cells and introduces potentially novel signaling pathways in dermal Papilla cells.

Rooster feathering, androgenic alopecia, and hormone-dependent tumor growth: what is in common?

This work surveys sex hormone-regulated morphogenetic processes in various epithelial organs and shows exemplary data of differences in their growth rate, proliferative cell population, and signaling molecule expression.

Premature senescence of balding dermal papilla cells in vitro is associated with p16(INK4a) expression.

Premature senescence of balding DPC in vitro in association with expression of p16(INK4a)/pRB suggests that baldingDPC are sensitive to environmental stress and identifies alternative pathways that could lead to novel therapeutic strategies for treatment of AGA.

MicroRNAs take part in pathophysiology and pathogenesis of Male Pattern Baldness

Seven microRNAs are selected, predicted bioinformatically on a reverse engineering basis, from previously published microarray gene expression data and analyzed their expression in balding relative to non-balding dermal papillas and found for the first time upregulation of four micro RNAs that could participate in pathogenesis of MPB.



Do androgens influence hair growth by altering the paracrine factors secreted by dermal papilla cells?

The current focus lies in identifying specific factors produced, e.g. IGF-I and stem cell factor, and comparing their expression in cells from follicles with varying responses to androgen stimulation in vitro, to lead to greater understanding of androgen action and enable the development of better treatment for androgen-potentiated disorders.

Differences in testosterone metabolism by beard and scalp hair follicle dermal papilla cells

This study was designed to investigate whether cultured human dermal papilla cells contain 5α‐reductase and whether the metabolic capacity varies with the body site of the follicle in line with the clinical picture.

Balding hair follicle dermal papilla cells contain higher levels of androgen receptors than those from non-balding scalp.

Higher levels of androgen receptors in cells from balding scalp hair follicles with similar properties to those from non-balding scalp concur with the expectations from their in vivo responses to androgens, and supports the hypothesis that androgens act via the dermal papilla.

Cultured dermal papilla cells from androgen-dependent human hair follicles (e.g. beard) contain more androgen receptors than those from non-balding areas of scalp.

Cells from androgen-sensitive follicles (beard, scrotum and pubis) contained higher levels of androgen receptors than those derived from relatively androgens-insensitive non-balding scalp follicles whether the receptor content was calculated in relation to cell number, protein or DNA content of the cells.

The metabolism of testosterone by dermal papilla cells cultured from human pubic and axillary hair follicles concurs with hair growth in 5 alpha-reductase deficiency.

The pubic and axillary cell results contrasts with the observations of pronounced 5 alpha-dihydrotestosterone in beard cells and confirm that androgen metabolism in cultured dermal papilla cells reflects the parent follicle's ability to respond to androgen in the absence of 5alpha-reductase type II in vivo.

Androgens and human hair growth

This review summarizes the present understanding of the structure and function of the human hair follicle and its hormonal regulation, particularly by androgens and discusses androgen dependent clinical conditions of hair growth and their treatment.

A comparison of the culture and growth of dermal papilla cells from hair follicles from non‐balding and balding (androgenetic alopecia) scalp

Male pattern baldness is a common, androgen‐dependent skin problem in adult men which is not well understood, although androgens are believed to act on the hair follicle via the mesenchyme‐derived dermal papilla, which may provide a useful in vitro model system.

Differences in hair follicle dermal papilla volume are due to extracellular matrix volume and cell number: implications for the control of hair follicle size and androgen responses.

A stereologic study on 235 hair follicles from different sites implies that the increase in the volume of the dermal papilla in these follicles is due to an increase inThe number of cells, either through proliferation or through the migration of cells from the follicular dermal sheath, and to an increases in the amount of extracellular matrix per cell.

Dermal papilla cells derived from beard hair follicles secrete more stem cell factor (SCF) in culture than scalp cells or dermal fibroblasts.

The hypotheses that the dermal papilla is a local source of SCF in hair follicles and that androgens would alter SCF production only at specific points of the hair cycle are supported.

Geometric relationships between the matrix of the hair bulb and its dermal papilla in normal and alopecic scalp.

The growth of hair appears to be intimately dependent upon the connective tissue papilla enveloped by the hair bulb, and it is observed that the matrix of the hair in mice does not differentiate, nor does proliferation of hair occur, if the cells of the papilla are destroyed with benzpyrene or methylcholan-threne.