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Genomics 2003 Jan;81(1):6-14
Curly bare (cub), a new mouse mutation on chromosome 11 causing skin and hair abnormalities, and a modifier gene (mcub) on chromosome 5.
In the outcrossing of a new recessive mouse mutation causing hair loss, a new wavy-coated phenotype appeared. The two distinct phenotypes were shown to be alternative manifestations of the same gene mutation and attributable to a single modifier locus. The new mutation, curly bare (cub), was mapped to distal Chr 11 and the modifier (mcub) was mapped to Chr 5. When homozygous for the recessive mcub allele, cub/cub mice appear hairless. A single copy of the dominant Mcub allele confers a full, curly coat in cub/cub mice. Reciprocal transfer of full-thickness skin grafts between mutant and control animals showed that the skin phenotype was tissue autonomous. The hairless cub/cub mcub/mcub mice show normal contact sensitivity responses to oxazolone. The similarity of the wavy coat phenotype to those of Tgfa and Egfr mutations and the map positions of cub and mcub suggest candidate genes that interact in the EGF receptor signal transduction pathway.
Clin Exp Dermatol 2002 Jul;27(5):396-404
Nutritional factors and hair loss.
The literature reveals what little is known about nutritional factors and hair loss. What we do know emanates from studies in protein-energy malnutrition, starvation, and eating disorders. In otherwise healthy individuals, nutritional factors appear to play a role in subjects with persistent increased hair shedding. Hard, 40 years ago, demonstrated the importance of iron supplements in nonanaemic, iron-deficient women with hair loss. Serum ferritin concentrations provide a good assessment of an individual's iron status. Rushton et al. first published data showing that serum ferritin concentrations were a factor in female hair loss and, 10 years later, Kantor et al. confirmed this association. What level of serum ferritin to employ in subjects with increased hair shedding is yet to be definitively established but 70 micro g/L, with a normal erythrocyte sedimentation rate (< 10 mm/h), is recommended. The role of the essential amino acid, l-lysine in hair loss also appears to be important. Double-blind data confirmed the findings of an open study in women with increased hair shedding, where a significant proportion responded to l-lysine and iron therapy. There is no evidence to support the popular view that low serum zinc concentrations cause hair loss. Excessive intakes of nutritional supplements may actually cause hair loss and are not recommended in the absence of a proven deficiency. While nutritional factors affect the hair directly, one should not forget that they also affect the skin. In the management of subjects with hair loss, eliminating scaling problems is important as is good hair care advice and the need to explain fully the hair cycle. Many individuals reduced their shampooing frequency due to fear of losing more hair but this increases the amount seen in subsequent shampoos fuelling their fear of going bald and adversely affecting their quality of life.
Clin Exp Dermatol 2002 Jul;27(5):373-82
Male androgenetic alopecia.
Androgenetic alopecia (AGA) is the most common type of hair loss in men. The relative strong concordance of the degree of baldness in fathers and sons is not consistent with a smiple Mendelian trait and a polygenic basis is considered to be most likely. So far the predisposing genes for AGA are unknown and we do not understand the molecular steps involved in androgen-dependent beard growth versus androgen-dependent hair loss, but AGA can be defined as a DHT-dependent process with continuous miniaturization of sensitive hair follicles. The type 2 5aR plays a central role by the intrafollicular conversion of T to DHT. Due to the inceasing knowledge in this field, this article shall privide an critical overwiew of recent discoveries.
Cell Struct Funct. 2003 Feb;28(1):97-104.
Autoimmune hair loss induced by alloantigen in C57BL/6 mice.
Exponentially growing Meth-A cells expressing H-2K(d).D (d) antigen were found to induce alopecia when injected intraperitoneally into normal C57BL/6 mice, which express the H-2K(b).D (b) antigen. However, the capacity to induce alopecia disappeared when Meth-A cells were treated with K252a, which inhibits protein kinases. Histologically, skin in affected areas showed dense mononuclear cell infiltration and a focal foreign-body giant-cell reaction in hair follicles. The subtyping of lymphocytes in peripheral blood demonstrated a significant difference between normal mice and Meth-A cell-injected mice. To further examine the mechanism by which the alloantigen induces alopecia, lymphocytes isolated from the peripheral blood of normal C57BL/6 mice were cultured in medium containing Meth-A cell homogenate, phytohemagglutinin (PHA) and recombinant mouse interleukin-2 (rm IL-2), and intravenously injected into normal C57BL/6 mice. The adoptive transfer of the lymphocytes induced alopecia in a similar way. These findings suggest that the protein kinase-modulated alloantigen induces alopecia by disturbing the immunological homeostasis, and that lymphokine-activated killer cells play an important role in induction of alopecia by cross-reacting with hair follicles.
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