Hair density, hair diameter and the prevalence of female pattern hair loss.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Using RNA in situ hybridization analysis, we have characterized the expression domains of the four known members of the FGF receptor-tyrosine kinase gene family in the murine hair follicle at various stages of the hair growth cycle. During anagen, we detected Fgfr1 RNA in the dermal papilla, Fgfr2 RNA in hair matrix cells near the dermal papilla, Fgfr3 RNA in pre-cuticle cells in the periphery of the hair bulb, and Fgfr4 RNA in cells in the periphery of the hair bulb and also in the inner and outer root sheath in the lower half of the follicle neck. No RNA expression of these genes was detected during late catagen or telogen. We have previously shown that Fgf5 is expressed in the outer root sheath in the transient portion of the follicle (Hébert et al. [1994] Cell 78:1017-1025). In the present study we have also assayed for the expression of six other members of the FGF ligand gene family, Fgf3, Fgf4, Fgf6, Fgf7, Fgf8, and Fgf9. Among these FGF genes, only Fgf7 was found to be expressed in the hair follicle. Fgf7 RNA is localized to the dermal papilla during anagen, but expression is down-regulated by the late-anagen VI stage. We have also demonstrated that addition of FGF5 protein to the culture medium changes the behavior of dermal papilla cells in vitro, indicating that they are capable of responding to FGF5. Together with previously published data, these results provide a complete analysis of FGF ligand and FGF receptor-tyrosine kinase gene expression in the hair follicle, and suggest that FGF signalling may have several functions in the hair growth cycle.
The Cu and Zn levels of both 607 men (1-85 y old) and 649 women (1-92 y old) were determined by atomic absorption spectrometry. Sex does not influence Cu (14.89 + or - 0.89 mu g/g and 15.26 + or - 0.79 mu g/g hair for males and females, respectively) and Zn contents (200.97 + or - 9.68 mu g/g for men and 209.81 + or - 9.49 mu g/g hair for women). Age influences Cu and Zn concentrations, but only significantly in females: Cu levels decrease over 60 y of age; whereas Zn levels increase significantly from age groups 2-5 to 20-40 years. Hair color influences Cu concentrations in both males and females. In males, white hair contains less Cu than black hair; in females, white hair's Cu levels are significantly lower than those of dark blond, red, light brown, and brown hair. There are no significant differences in Zn concentrations with respect to different hair colors, in either males or females.
Monilethrix is a rare dominant hair disease characterized by beaded or moniliform hair which results from the periodic thinning of the hair shaft and shows a high propensity to excess weathering and fracturing. Several cases of monilethrix have been linked to the type II keratin gene cluster on chromosome 12q13 and causative heterozygous mutations of a highly conserved glutamic acid residue (Glu 410 Lys and Glu 410 Asp) in the helix termination motif of the type II hair keratin hHb6 have recently been identified in monilethrix patients of two unrelated families. In the present study, we have investigated two further unrelated monilethrix families as well as a single case. Affected members of one family and the single patient exhibited the prevalent hHb6 Glu 410 Lys mutation. In the second family, we identified in affected individuals a lysine substitution of the corresponding glutamic acid residue, Glu 403, in the type II hair keratin hHb1, suggesting that this site represents a mutational hotspot in these highly related type II hair keratins. Both hHb1 and hHb6 are largely coexpressed in cortical trichocytes of the hair shaft. This indicates that monilethrix is a disease of the hair cortex.
The authors report on a laboratory model for continuous production of human hair during long periods of time. This study shows that the amino acid composition of hairs collected in situ from human scalp was similar to that of terminal hairs produced by the donors' scalp follicles grafted and maintained onto nude mice. A similar experiment was performed with scalp samples from a foetus with trichothiodystrophy (TTD). The amino acid analysis of TTD lanugo hairs and of the TTD shafts produced by grafted scalp specimens was consistent with findings published in the literature: severe decrease of cys (< 50% of control values) and moderate decrease of thr and pro (80% of control values or less) with an increase of ala-asp-ile-leu-lys-met-phe (120% of control values or more). These changes indicate a decrease of high sulphur proteins (HSP) and consequently a relative increase of keratins. Furthermore, when foetal scalp samples were grafted, the lanugo hairs transformed into terminal hairs along with normal initiation of melanisation. Hence, keratin and HSP gene expression and regulation of melanogenesis in the normal and genetically defective TTD human hair follicle grafts appear to be independent of systemic host-related factors, at least during a 6 months follow-up period after grafting. The present experimental evidence further supports conclusions gained from previous assays with normal and TTD variant scalp grafts, i.e. that the nude mouse bearing human scalp specimens may serve as a clinically relevant laboratory model for evaluating regulation of normal and abnormal gene expression in the hair follicle under well controlled experimental conditions.
Here, we provide the first study of prolactin (PRL) and prolactin receptor (PRLR) expression during the nonseasonal murine hair cycle, which is, in contrast to sheep, comparable with the human scalp and report that both PRL and PRLR are stringently restricted to the hair follicle epithelium and are strongly hair cycle-dependent. In addition we show that PRL exerts functional effects on anagen hair follicles in murine skin organ culture by down-regulation of proliferation in follicular keratinocytes. In telogen follicles, PRL-like immunoreactivity was detected in outer root sheath (ORS) keratinocytes. During early anagen (III to IV), the developing inner root sheath (IRS) and the surrounding ORS were positive for PRL. In later anagen stages, PRL could be detected in the proximal IRS and the inner layer of the ORS. The regressing (catagen) follicle showed a strong expression of PRL in the proximal ORS. In early anagen, PRLR immunoreactivity occurred in the distal part of the ORS around the developing IRS, and subsequently to a restricted area of the more distal ORS during later anagen stages and during early catagen. The dermal papilla (DP) stayed negative for both PRL and PRLR throughout the cycle. Telogen follicles showed only a very weak PRLR staining of ORS keratinocytes. The long-form PRLR transcript was shown by real-time polymerase chain reaction to be transiently down-regulated during early anagen, whereas PRL transcripts were up-regulated during mid anagen. Addition of PRL (400 ng/ml) to anagen hair follicles in murine skin organ culture for 72 hours induced premature catagen development in vitro along with a decline in the number of proliferating hair bulb keratinocytes. These data support the intriguing concept that PRL is generated locally in the hair follicle epithelium and acts directly in an autocrine or paracrine manner to modulate the hair cycle.
During anagen, cell proliferation in the germinative matrix of the hair follicle gives rise to the fiber and inner root sheath. The hair fiber is constructed from structural proteins belonging to four multigene families: keratin intermediate filaments, high-sulfur matrix proteins, ultra high-sulfur matrix proteins, and high glycine-tyrosine proteins. Several hair-specific keratin intermediate filament proteins have been characterized, and all have relatively cysteine-rich N- and C-terminal domains, a specialization that allows extensive disulfide cross-linking to matrix proteins. We have cloned two complete type II hair-specific keratin genes (ghHb1 and ghHb6). Both genes have nine exons and eight introns spanning about 7 kb and lying about 10 kb apart. The structure of both genes is highly conserved in the regions that encode the central rod domain but differs considerably in the C-terminal coding and noncoding sequences, although some conservation of introns does exist. These genes have been localized to the type II keratin cluster on chromosome 12q13 by fluorescence in situ hybridization. They, and their type I partner ghHa1, are expressed in differentiating hair cortical cells during anagen. In cultured follicles, ghHa1 expression declined in cortical cells and was no longer visible after 6 d, whereas the basal epidermal keratin hK14 appeared in the regressing matrix. The transition from anagen to telogen is marked by downregulation of hair cortical specific keratins and the appearance of hK14 in the epithelial sac to which the telogen hair fiber is anchored. Further studies of the regulation of these genes will improve our understanding of the cyclical molecular changes that occur as the hair follicle grows, regresses, and rests.
To establish a model for studying human scalp hair, individually isolated hair follicles were grafted onto back skin of severe combined immunodeficient mice. Histologic changes and cell kinetics in the hair loss and subsequent recovery process were investigated. In the dystrophic stage (from day 7 to 30), all the hair shafts became dystrophic and were shed. Thickening and corrugation of vitreous membrane, apoptosis, and regression of the lower part were observed in the grafted hair follicles. 5-bromo-2'-deoxy-uridine-labeled cells were not detected in the lower end of the follicles, and keratin 19-positive cells appeared there. At the end of this stage their lower part was maximally retracted, secondary germ remained beneath the bulge, and the vitreous membrane disappeared. In the regeneration stage (from day 30 to 50), the same histologic findings as those at the end of the dystrophic stage were observed. The keratin 19-positive cells in the secondary germ, however, were replaced with keratin 19-negative and 5-bromo-2'-deoxy-uridine-labeled cells. Then, differentiation into an inner root sheath and a hair shaft began, and apoptosis was terminated. In the stable growth stage (from day 40 to at least 150), the grafted follicles were immunohistochemically and light microscopically identical with the normal anagen hair follicles except for the presence of melanin incontinence. These findings suggest that the grafted hair follicles entered into dystrophic catagen, subsequently dystrophic telogen, then returned to normal anagen follicles, and that stem cells or their close progeny in the secondary germ play an important part in the recovery process.