Curly bare (cub), a new mouse mutation on chromosome 11 causing skin and hair abnormalities, and a modifier gene (mcub) on chromosome 5.

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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.

Development 2003 Jan;130(2):379-89

'Cyclic alopecia' in Msx2 mutants: defects in hair cycling and hair shaft differentiation.

Msx2-deficient mice exhibit progressive hair loss, starting at P14 and followed by successive cycles of wavelike regrowth and loss. During the hair cycle, Msx2 deficiency shortens anagen phase, but prolongs catagen and telogen. Msx2-deficient hair shafts are structurally abnormal. Molecular analyses suggest a Bmp4/Bmp2/Msx2/Foxn1 acidic hair keratin pathway is involved. These structurally abnormal hairs are easily dislodged in catagen implying a precocious exogen. Deficiency in Msx2 helps to reveal the distinctive skin domains on the same mouse. Each domain cycles asynchronously - although hairs within each skin domain cycle in synchronized waves. Thus, the combinatorial defects in hair cycling and differentiation, together with concealed skin domains, account for the cyclic alopecia phenotype.

Zhonghua Zheng Xing Wai Ke Za Zhi 2002 Jul;18(4):219-20

Dense-packing hair grafting technique for restoration of cicatricial alopecia

OBJECTIVE: To investigate the possibility of using dense-packing hair grafting technique for restoration of cicatricial alopecia. METHODS: Under local anesthesia, a scalp strip was harvested from the back of the head. A series of micro-grafts with 1-3 hairs and mini-grafts with 4-6 hairs were created from this strip. In the scarring recipient area, micro-slots were made with a 18 G needle for the micro-grafts and mini-slits were made with a No. 64 mini-blade for the mini-grafts. The grafts were then implanted into these holes. RESULTS: Ninety-six patients with 128 bald scarring areas, resulted from burn, trauma or infection, were treated with the above-mentioned technique from April. 1998 to February. 2000. All of the patients were satisfied with the appearance. In the micro-graft area, the graft density reached 10-15 mini-grafts/cm2 per session. In the micro-graft area, the graft density reached 16-19 micro-grafts/cm2 per session. Postoperative following-up for more than 1 year showed that the grafted hairs were growing well with 90%-95% survival of the hair. One third of the patients obtained satisfactory results with only one session. Two thirds of the patients needed the second session to improve the appearance. CONCLUSIONS: The dense-packing hair grafting technique is a simple, safe and effective method for hair restoration surgery. It is not only used for male pattern baldness, but could also be applied for restoration of cicatricial alopecia.

J Dermatol Sci 2002 Aug;29(2):85-90

Antioxidant enzymes and lipid peroxidation in the scalp of patients with alopecia areata.

Alopecia areata (AA) is an autoimmune inflammatory disease. However, little is known about the alterations in lipid peroxidation and antioxidant enzymes in the scalp of patients with AA. Therefore, the aim of this study was to investigate the status of oxidative stress in the scalp of patients with AA. We measured the levels of thiobarbituric acid reactive substances (TBARS) as lipid peroxidation status, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as antioxidant enzymes in the scalp of ten patients with AA and ten control subjects. The levels of TBARS in scalp of patients with AA (3654.1+/-621.2 nmol/g tissue) were significantly higher than those of controls (1210.2+/-188.8 nmol/g tissue) (P=0.002). The levels of SOD (134.8+/-23.8 U/g tissue) and GSH-Px (332.7+/-66.2 U/g tissue) in scalp of patients with AA were also significantly higher than those of controls (63.2+/-8.8 U/g tissue, 112.0+/-18.4 U/g tissue, respectively) (P=0.019, P=0.002, respectively). The mean levels of TBARS, SOD and GSH-Px in early phase of disease were increased 2-fold as compared with late phase of the disease. These results indicate that oxidative status is affected in AA. Lipid peroxidation and antioxidant enzymes may be involved in the pathogenesis of AA. Furthermore, we found high SOD and GSH-Px activities in the scalp of patient with AA. These high levels could not protect the patients against the reactive oxygen species, because lipid peroxidation could not be lowered in AA patients.

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