Human hair growth in vitro: a model for the study of hair follicle biology

Philpott, Michael P.; Sanders, Deborah A.; Westgate, Gillian; Kealey, Terence

doi:10.1016/0923-1811(94)90036-1

Cited by 122 publications

(135 citation statements)

References 57 publications

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“…The first phase of hair follicle development is called postnatal hair follicle morphogenesis. Studies with TGF-β1 null mice further support the hypothesis that TGF-β1 plays an important role in catagen induction (Foitzik et al, 2000;Philpott et al, 1994;Soma et al, 1998). Consistent with this possibility, TGF-β and TGF-β receptor type II expression is maximal at the anagencatagen transition Welker et al, 1997).…”

supporting

confidence: 65%

“…The length of the hair shaft depends primarily on the number of days that a follicle remains in anagen (Stenn and Paus, 2001). This fact and the proposed involvement of TGF-β in the onset of catagen (Foitzik et al, 2000;Paus et al, 1997;Philpott et al, 1994;Seiberg et al, 1995;Soma et al, 2003;Soma et al, 1998;Welker et al, 1997) suggested that the duration of anagen might be modified in the ECR3E-Myc mice due to altered levels of active TGF-β. This hypothesis was evaluated by histological examination of the follicular morphogenesis in transgenic and wild-type mice during the first hair cycle.…”

Section: Early Induction Of Catagenmentioning

confidence: 99%

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Expression of truncated latent TGF-β-binding protein modulates TGF-β signaling

Mazzieri

Jurukovski

Obata

et al. 2005

Journal of Cell Science

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Transforming growth factor-β is released from most cells as an inactive complex consisting of transforming growth factor-β, the transforming growth factor-β propeptide and the latent transforming growth factor-β-binding protein. We studied the role of latent transforming growth factor-β-binding protein in modulating transforming growth factor-β availability by generating transgenic mice that express a truncated form of latent transforming growth factor-β-binding protein-1 that binds to transforming growth factor-β but is missing the known N- and C-terminal matrix-binding sequences. As transforming growth factor-β is an inhibitor of keratinocyte proliferation and is involved in the control of hair cycling, we over-expressed the mutated form of latent transforming growth factor-β-binding protein under the control of the keratin 14-promoter. Transgenic animals displayed a hair phenotype due to a reduction in keratinocyte proliferation, an abbreviated growth phase and an early initiation of the involution (catagen) phase of the hair cycle. This phenotype appears to result from excess active transforming growth factor-β, as enhanced numbers of pSmad2/3-positive nuclei are observed in transgenic animal skin. These data suggest that the truncated form of latent transforming growth factor-β-binding protein-1 competes with wild-type latent transforming growth factor-β-binding protein for binding to latent transforming growth factor-β, resulting in latent transforming growth factor-β complexes that fail to be targeted correctly in the extracellular matrix. The mis-localization of the transforming growth factor-β results in inappropriate activation and premature initiation of catagen, thereby illustrating the significance of latent transforming growth factor-β-binding protein interaction with transforming growth factor-β in the targeting and activation of latent transforming growth factor-β in addition to previously reported effects on small latent complex secretion.

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supporting

confidence: 65%

Section: Early Induction Of Catagenmentioning

confidence: 99%

Expression of truncated latent TGF-β-binding protein modulates TGF-β signaling

Mazzieri

Jurukovski

Obata

et al. 2005

Journal of Cell Science

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“…41 The total number of organcultured HFs in anagen VI stage was 180, derived from 12 different individuals 25 to 55 years of age. After separation of epidermis and dermis from subcutaneous fat under a binocular dissecting microscope, anagen HFs were isolated from the subcutis by using watchmaker's forceps.…”

Section: Isolation and Culture Of Human Hair Folliclesmentioning

confidence: 99%

Human Scalp Hair Follicles Are Both a Target and a Source of Prolactin, which Serves as an Autocrine and/or Paracrine Promoter of Apoptosis-Driven Hair Follicle Regression

Foitzik

Krause

Conrad

et al. 2006

The American Journal of Pathology

133

171

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The prototypic pituitary hormone prolactin (PRL) exerts a wide variety of bioregulatory effects in mammals and is also found in extrapituitary sites, including murine skin. Here, we show by reverse transcriptase-polymerase chain reaction and immunohistology that, contrary to a previous report, human skin and normal human scalp hair follicles (HFs), in particular, express both PRL and PRL receptors (PRL-R) at the mRNA and protein level. PRL and PRL-R immunoreactivity can be detected in the epithelium of human anagen VI HFs, while the HF mesenchyme is negative. During the HF transformation from growth (anagen) to apoptosisdriven regression (catagen), PRL and PRL-R immunoreactivity appear up-regulated. Treatment of organ-cultured human scalp HFs with high-dose PRL (400 ng/ml) results in a significant inhibition of hair shaft elongation and premature catagen development, along with reduced proliferation and increased apoptosis of hair bulb keratinocytes (Ki-67/terminal dUTP nick-end labeling immunohistomorphometry). This shows that PRL receptors, expressed in HFs, are functional and that human skin and human scalp HFs are both direct targets and sources of PRL. Our data suggest that PRL acts as an autocrine hair growth modulator with catagenpromoting functions and that the hair growth-inhibitory effects of PRL demonstrated here may underlie the as yet ill-understood hair loss in patients with hyperprolactinemia.

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“…41 Control hair follicles were cultured with vehicle for 4 days. Test groups were treated with 75 IU/ml IFN-␥ (Peprotech, Rocky Hill, NJ) for 4 days.…”

Section: Hair Follicle Organ Culturementioning

confidence: 99%

Collapse and Restoration of MHC Class-I-Dependent Immune Privilege

Ito

Bettermann

et al. 2004

The American Journal of Pathology

244

322

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The collapse of major histocompatiblity complex (MHC) class-I-dependent immune privilege can lead to autoimmune disease or fetal rejection. Pragmatic and instructive models are needed to clarify the as yet obscure controls of MHC class I down-regulation in situ, to dissect the principles of immune privilege generation, maintenance, and collapse as well as to develop more effective strategies for immune privilege restoration. Here, we propose that human scalp hair follicles, which are abundantly available and easily studied, are ideally suited for this purpose: interferon-␥ induces ectopic MHC class I expression in the constitutively MHC class-I-negative hair matrix epithelium of organ-cultured anagen hair bulbs, likely via interferon regulatory factor-1, along with up-regulation of the MHC class I pathway molecules ␤ 2 microglobulin and transporter associated with antigen processing (TAP-2). In the first report to identify natural immunomodulators capable of down-regulating MHC class I expression in situ in a normal, neuroectoderm-derived human tissue, we show that ectopic MHC class I expression in human anagen hair bulbs can be normalized by treatment with ␣-MSH, IGF-1, or TGF-␤1, all of which are locally generated, as well as by FK506. These agents are promising candidates for immune privilege restoration and for suppressing MHC class I expression where this is clinically desired (eg, in alopecia areata, multiple sclerosis, autoimmune uveitis, mumps orchitis, and fetal or allograft rejection). A select number of mammalian tissue sites, namely the brain, cornea, anterior chamber of the eye, testis, liver, fetotrophoblast, and the hamster cheek pouch, display a fascinating phenomenon called "immune privilege." [1][2][3][4][5] This name reflects that these tissue environments can award allotransplants relative protection from rejection by the host immune system.

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Human hair growth in vitro: a model for the study of hair follicle biology

Cited by 122 publications

References 57 publications

Expression of truncated latent TGF-β-binding protein modulates TGF-β signaling

Expression of truncated latent TGF-β-binding protein modulates TGF-β signaling

Human Scalp Hair Follicles Are Both a Target and a Source of Prolactin, which Serves as an Autocrine and/or Paracrine Promoter of Apoptosis-Driven Hair Follicle Regression

Collapse and Restoration of MHC Class-I-Dependent Immune Privilege

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