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Curr Biol 2003 Feb 18;13(4):333-8
Notch/RBP-J Signaling Regulates Epidermis/Hair Fate Determination of Hair Follicular Stem Cells.
Notch signaling is involved in the cell fate determination of various cell lineages. Notch interaction with its ligand induces the cleavage of its intracellular domain (IC), and the Notch IC translocates to the nucleus and binds to RBP-J to transactivate transcription of target genes. All four Notches in mammals bind to RBP-J to exert their transactivation activities. Notch is expressed in developing or differentiating epidermis and hairs, inhibits the terminal differentiation of the epidermis, and regulates hair differentiation. The common stem cells that reside in the upper portion of hair follicles (the bulge) contribute to epidermal and hair cell formation. However, it is unknown what determines whether hair follicular stem cells will become hairs or epidermis. Here we report that conditionally disrupting the mouse RBP-J gene in a mosaic pattern to avoid embryonic lethality of RBP-J-deficiency caused hair loss, epidermal hyperkeratinization, and epidermal cyst formation. Cyst formation is probably due to a combination of the aberrant fate determination of RBP-J-deficient stem cells to epidermal progenitors and their accelerated differentiation into epidermis. These results suggest that Notch/RBP-J signaling regulates the cell fate determination of hair follicular stem cells at the bulge region.
Saudi Med J 2002 Dec;23(12):1489-91
Striae distensae - like lesions. A cause of scarring alopecia among children.
OBJECTIVE: Although alopecia areata is a common problem among children, many misdiagnoses for this condition can happen. The aim of this study was to demonstrate the striae distensae as lesions that cause scarring alopecia with a great resemblance to alopecia areata. METHODS: A total of 36 children with provisional diagnosis of alopecia areata of the scalp were assessed clinically in the Department of Dermatology and Venereology, Baghdad Teaching Hospital, Baghdad, Iraq, between June 1998 to June 2001. Their age ranged from 3 12 years and the mean + standard deviation (SD) was 7.30 + 2.59 years with equal sex ratio. RESULTS: All patients provided for this study had a history of patchy hair loss of few months duration. Their parents denied any history of obvious trauma and many modalities of treatment had been tried without benefit. The clinical examination revealed single or multiple (1-6) (mean + SD 2.41 + 1.22) complete linear hair loss patches resembling atrophic scar that was similar to striae distensae. The histopathological examination showed atrophy of the epidermis, full replacement of the dermis by collagen bundles, and complete loss of appendages. CONCLUSION: This is a new entity, which seems to be common among children and often confused with untreated cases of alopecia areata. This condition should be added to the differential diagnosis of patchy hair loss in children and the parents should be reassured of the cause of hair loss and no treatment therapy needed.
J Am Acad Dermatol 2002 Apr;46(4):517-23
Changes in hair weight and hair count in men with androgenetic alopecia after treatment with finasteride, 1 mg, daily.
BACKGROUND: Finasteride, a type II 5alpha-reductase inhibitor, reduces scalp and serum dihydrotestosterone and has been shown to be effective in men with androgenetic alopecia (AGA). OBJECTIVE: The purpose of this study was to determine the effect of finasteride on scalp hair weight in men with AGA. METHODS: Sixty-six men with AGA received finasteride, 1 mg/d, or placebo in a 48-week study, and 49 men continued in a 48-week extension. Efficacy was assessed by scalp hair weights and hair counts. RESULTS: As expected, hair counts improved with finasteride (net mean percent change +/- SE [95% CI] compared with placebo = 9.2% +/- 2.8% [3.8, 14.6] and 15.4% +/- 3.2% [9.1, 21.7] at 48 and 96 weeks, respectively; P <.01 for both time points), and net improvements in hair weight were greater (25.6% +/- 3.6% [18.5, 32.7] and 35.8% +/- 4.6% [26.7, 44.8] at 48 and 96 weeks, respectively; P <.001 for both time points). Finasteride was generally well tolerated. CONCLUSION: In this study, finasteride, 1 mg, increased hair weight in men with AGA. Hair weight increased to a larger extent than hair count, implying that factors other than the number of hairs, such as increased growth rate (length) and thickness of hairs, contribute to the beneficial effects of finasteride in treated men.
Am J Pathol. 2003 Mar;162(3):803-14.
Stress inhibits hair growth in mice by induction of premature catagen development and deleterious perifollicular inflammatory events via neuropeptide substance P-dependent pathways.
It has been much disputed whether or not stress can cause hair loss (telogen effluvium) in a clinically relevant manner. Despite the paramount psychosocial importance of hair in human society, this central, yet enigmatic and controversial problem of clinically applied stress research has not been systematically studied in appropriate animal models. We now show that psychoemotional stress indeed alters actual hair follicle (HF) cycling in vivo, ie, prematurely terminates the normal duration of active hair growth (anagen) in mice. Further, inflammatory events deleterious to the HF are present in the HF environment of stressed mice (perifollicular macrophage cluster, excessive mast cell activation). This provides the first solid pathophysiological mechanism for how stress may actually cause telogen effluvium, ie, by hair cycle manipulation and neuroimmunological events that combine to terminate anagen. Furthermore, we show that most of these hair growth-inhibitory effects of stress can be reproduced by the proteotypic stress-related neuropeptide substance P in nonstressed mice, and can be counteracted effectively by co-administration of a specific substance P receptor antagonist in stressed mice. This offers the first convincing rationale how stress-induced hair loss in men may be pharmacologically managed effectively.
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