Control of murine hair follicle regression (catagen) by TGF‐β1<i>in vivo</i>

Foitzik, Kerstin; Lindner, G; Mueller-Roever, Sven; Maurer, Marcus; Botchkareva, Natasha; Botchkarev, Vladimir A.; Handjiski, Bori; Metz, Martin; Hibino, Toshihiko; Soma, Tsutomu; Dotto, G. Paolo; Paus, Ralf

doi:10.1096/fasebj.14.5.752

Cited by 324 publications

(331 citation statements)

References 40 publications

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“…Our studies now allow a careful dissection of potential interactions͞cross-talk between wnt signaling and other genetic pathways that play a role in differentiation of the hair follicle. In this context, it is interesting to note that (i) several CAGA-or GTCT-like sequences, to which Smad proteins, intracellular signaling mediators of transforming growth factor-␤ (TGF-␤) pathways, bind (41), are present in the movo1 promoter, (ii) LEF1 and Smad have been shown to interact and regulate gene expression in a coordinated manner to integrate wnt and TGF-␤ signals (42,43), and (iii) TGF-␤s are known to play important roles in hair follicle development (44)(45)(46). …”

Section: Discussionmentioning

confidence: 99%

The LEF1/β-catenin complex activates movo 1, a mouse homolog of Drosophila ovo required for epidermal appendage differentiation

Mackay

Dai

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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Drosophila ovo͞svb (dovo) is required for epidermal cuticle͞den-ticle differentiation and is genetically downstream of the wg signaling pathway. Similarly, a mouse homolog of dovo, movo1, is required for the proper formation of hair, a mammalian epidermal appendage. Here, we provide biochemical evidence that movo1 encodes a nuclear DNA binding protein (mOvo1a) that binds to DNA sequences similar to those that dOvo binds to, further supporting the notion that mOvo1a and dOvo are genetically and biochemically homologous proteins. Additionally, we show that the movo1 promoter is activated by the lymphoid enhancer factor 1 (LEF1)͞␤-catenin complex, a transducer of wnt signaling. Collectively, our findings suggest that movo1 is a developmental target of wnt signaling during hair morphogenesis in mice, and that the wg͞wnt-ovo link in epidermal appendage regulatory pathways has been conserved between mice and flies.hair follicle ͉ wnt ͉ wg ͉ mouse ovo1

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Section: Discussionmentioning

confidence: 99%

The LEF1/β-catenin complex activates movo 1, a mouse homolog of Drosophila ovo required for epidermal appendage differentiation

Mackay

Dai

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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“…From a literature-based approach, we examined the expression levels of six important hair cycle regulators: Fgf5 (30), Tgf␣ (35,36), Egf (37), PTHrP (38), Tgf␤1 (39), and Msx2 (40). By quantitative real-time PCR before the onset of aberrant hair remodeling (day P11), we did not find significant changes in expression levels of these candidate genes between Barx2 Ϫ/Ϫ and control tissue, although some of them actually decreased (relative to wild type) with the onset of catagen at P15 (data not shown).…”

Section: Up-regulated Genes Identified In Barx2 Mutant Skin By Rna Prmentioning

confidence: 99%

Barx2 functions through distinct corepressor classes to regulate hair follicle remodeling

Olson

Zhang

Taylor

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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The hair-growth cycle, a complex biological system requiring coordinate alterations in gene expression and cellular behavior, provides a challenging model for investigating the interplay of specific transcriptional regulation events. Here we report that the Barx2 homeodomain factor serves as a regulator of hair follicle remodeling (catagen), and loss of Barx2 in mice causes a defect both in the initiation and progression of catagen, resulting in a protracted first catagen, and later, causing short hair in adult gene-deleted mice. Barx2 negatively regulates its own promoter, and our study highlights the role of Barx2 as a repressor in the skin that can, unexpectedly, functionally interact with two WD40-domain factors distantly related to the yeast corepressor Tup1. These two corepressors, transducin-like enhancer of split and transducin ␤-like 1, function through distinct and independent interactions with Barx2 for the repression of gene targets, including the Barx2 gene itself, emphasizing the roles of complementary repression strategies in engrailed homology-1 motif-containing homeodomain factors. Together, our data suggest that the hairremodeling defect of Barx2 mutant mice could be explained, in part, by failure to repress one or more critical target genes.A distinctive feature of the hair follicle is its periodic regeneration and degeneration throughout the lifetime of the organism in cycles of three phases: anagen, catagen, and telogen. In mice, hair follicle morphogenesis begins late in development and continues through growth, or anagen, of the first pelage until Ϸ2 weeks after birth. The final length of the hair is genetically determined by the period spent in anagen, with hair-generating cells of the bulb having a finite proliferative capacity that is influence by factors from the dermal papilla and surrounding tissues. Anagen terminates with the destruction of the growing part of the follicle in a remodeling process called catagen. Thereafter, a resting period, or telogen, intervenes with the finished hair normally retained in the diminutive follicle, until anagen reinitiates with the start of a new cycle of hair growth (1, 2). Two synchronous cycles of hair growth occur in juvenile mice, with consecutive waves of anagen-catagen-telogen moving from neck to tail, and thereafter only smaller patches of follicles cycle together in adult mice. From the human perspective, hair follicle remodeling is important because changes in the hair cycle underlie most disorders involving unwanted hair growth or loss (3, 4). Evidence is also emerging that hair cycling and wound healing share some basic molecular strategies (5).The transcriptional control of skin and hair development, and regulation of postnatal, cycling hair follicles, represents a complex system involving the coordinated actions of many intracellular signaling molecules and transcription factors. Recently, expression profiling has been used to systematically identify hair-cycle-associated genes and cluster them into major classes of expression over the...

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“…Others GFs exert their action through an inhibitory effect and down-regulation on hair growth and that may be involved in the beginning of the catagen phase [39]. Some of these GFs include: growth factor bone morphogenetic protein-4 (BMP-4), transforming growth factor-β (TGF-β), interleukin-1α (IL-1α) and tumour necrosis factor-α (TNF-α) [45,46].…”

Section: Anatomy and Hair Cyclementioning

confidence: 99%

Androgenetic Alopecia: a Review and Emerging Treatments

Alves¹

2017

CRDOA

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Androgenetic Alopecia (AGA) is the most common noncicatricial alopecia that leads to the progressive miniaturization of the hair follicle. Scalp terminal hairs are converted into vellus hairs, primarily due to two factors: genetic predisposition and hormonal stimulation.The incidence and prevalence of AGA increases with age. The onset of AGA is gradual, and when this pathology progresses, the anagen phase shortens and the telogen phase remains constant. The shedding area varies from patient to patient and is usually most marked at the vertex in men, while women with AGA generally lose hair diffusely over the crown.Topical minoxidil and oral finasteride (5-alpha-reductase type II inhibitor) are the gold-standard therapies for AGA and are currently the only Food and Drug Administration (FDA)-approved drugs for the treatment of AGA.The currently available treatments for AGA are sometimes perceived as having limited effectiveness; therefore, the identification of new therapies for this pathology is of utmost importance.This article aims to review the pathogenesis, diagnosis of AGA and all the new emerging treatments for this entity in order to prevent its progression and improve the results of this pathology.

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Control of murine hair follicle regression (catagen) by TGF‐β1in vivo

Cited by 324 publications

References 40 publications

The LEF1/β-catenin complex activates movo 1, a mouse homolog of Drosophila ovo required for epidermal appendage differentiation

The LEF1/β-catenin complex activates movo 1, a mouse homolog of Drosophila ovo required for epidermal appendage differentiation

Barx2 functions through distinct corepressor classes to regulate hair follicle remodeling

Androgenetic Alopecia: a Review and Emerging Treatments

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