Loss of cell adhesion in Dsg3bal-Pas mice with homozygous deletion mutation (2079del14) in the desmoglein 3 gene.

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J Invest Dermatol 2002 Dec;119(6):1237-43

Loss of cell adhesion in Dsg3bal-Pas mice with homozygous deletion mutation (2079del14) in the desmoglein 3 gene.

Pemphigus encompasses a group of autoimmune blistering diseases with circulating pathogenic autoantibodies recognizing several proteins, including the desmosomal cadherin, desmoglein 3. Targeted disruption of the Dsg3 gene by homologous recombination (Dsg3tm1stan) in mouse results in fragility of the skin and oral mucous membranes, analogous to the human disease. In addition, the Dsg3tm1stan mice develop phenotypic runting and hair loss, identical to that of the mouse mutant, Dsg3bal-2J. The Dsg3bal-2J mice are homozygous for a 1 bp insertion (2275insT) in the Dsg3 gene resulting in a nonfunctional Dsg3 mRNA. In this study, we characterized an allelic mutation, Dsg3bal-Pas, with clinical features similar to those in Dsg3bal-2J. We have identified a 14 bp deletion in exon 13 of the Dsg3 gene resulting in a frameshift and premature termination codon 7 bp downstream from the site of the deletion and causing a truncation of the desmoglein 3 polypeptide by 199 amino acids, eliminating virtually all of the intracellular domain. We demonstrate that, although a Dsg3 mRNA transcript was detectable in Dsg3bal-Pas skin, the corresponding protein for desmoglein 3 was completely absent in the oral mucosal epithelium of homozygous Dsg3bal-Pas compared with that of +/Dsg3bal-Pas mice. No significant changes in the expression of desmogleins 1 and 2 were detected. To elucidate a potential mechanism causing loss of cell adhesion in the Dsg3bal-Pas mice, we generated a myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein and expressed it in keratinocytes. The myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein was found predominantly in the cytoplasm possibly due to increased proteolytic degradation. Cell surface staining was also detected but was jagged, not linear along the cell-cell border like that observed for the full-length desmoglein 3. The expression of the myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein resulted in a reduction in staining of other desmosomal proteins, including desmoglein 1 and 2, plakophilin 2, and plakoglobin. In addition, the cells expressing myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein underwent dramatic changes in cell morphology and exhibited striking extensive filopodia. Collectively, these data showed that the perturbation of desmoglein 3 found in the Dsg3bal-Pas mice resulted in disadhesion of keratinocytes manifested with blistering phenotype.

Ann Dermatol Venereol 2002 May;129(5 Pt 2):841-4

The hair follicle as a target for gene therapy

The hair follicle possesses progenitor cells required for continuous hair follicle cycling and for epidermal keratinocytes, melanocytes and Langerhans cells. These different cell types can be the target of topical gene delivery in the skin of the mouse. Using a combination of liposomes and DNA, we demonstrate the feasibility of targeting hair follicle cells in human scalp xenografts. We consider liposome composition and stage of the hair cycle as important parameters influencing transfection of human hair follicles. Transfection is possible only during the early anagen phase. Factors and obstacles for the use of gene therapy in treating alopecia and skin diseases are discussed. A theoretical framework for future treatment of cutaneous and systemic disorders using gene therapy is presented.

Dermatology 2002;205(2):108-10

Kenogen. A new phase of the hair cycle?

BACKGROUND: A novel phenomenon has been described by the phototrichogram: the emptiness of the follicle after teloptosis. We called this phenomenon kenogen, from the Greek kappaepsilonnuovarsigma, 'empty'. OBJECTIVE: To describe the kenogen phase in its details. METHODS: Analysis of the existing literature. RESULTS: The original observation in 2 women was confirmed in 10 balding and non-balding males studied for 14 years in whom kenogen lasted about 4 months increasing up to about 7 months and affecting 80% of all hair cycles. In 2 women with progressing androgenetic alopecia studied for 2 years, kenogen involved 22% of the hair follicles, lasting from 3 months to 1 year. In a prepubertal boy studied for 1 year, it involved 8% of hairs and lasted about 2 months. CONCLUSION: During kenogen, the hair follicle rests physiologically, but duration and frequency are greater in androgenetic alopecia, possibly accounting for baldness. In addition to the classical cycle, the hair follicle may follow an alternative route during which the telogen phase, not accompanied by a coincident new early anagen, ends with teloptosis leaving the follicle empty.

Dermatol Surg 2002 May;28(5):394-400; discussion 401

A method for evaluating and treating the temporal peak region in patients with male pattern baldness.

BACKGROUND: In the past, hair restoration surgeons have focused most of their attention and efforts on the reconstruction of the hairline region and the area on top of the head. However, little attention has been given to the temporal peaks and the areas immediately posterior to them. OBJECTIVE: The goals of this article are to describe the pattern baldness process at the temporal peaks and the region immediately posterior to them, and to describe a method for the evaluation and treatment of these very important and often neglected areas. METHODS: A method for evaluating and grading the temporal peak region is given. A surgical technique for treating this problem is described. This method consists of making 1.0 mm spear blade incisions at a very acute 10 degrees angle in the newly designed anterior peak and in between the hair follicles that remain in the area posterior to the peak. The grafting of the finest one-haired grafts available in between existing hair follicles is accomplished with the help of 3.5x expandable loupes. The anterior temporal peak design is coordinated with the position of the frontal hairline restoration; the more anterior the hairline, the more anterior the temporal peak and vice-versa. RESULTS: The results of evaluating the temporal peak areas and treating them appropriately have consistently restored the cosmetic harmony between the frontal hairline and the temporal peak region. It is important, however, to only utilize the finest hairs available to create an aesthetically pleasing result. CONCLUSION: When evaluating patients for hair restoration surgery, it should be a common practice to evaluate the temporal peak regions and the areas immediately posterior to them. These areas should be appropriately treated so that the frontal hair restoration coordinates with that of the temporal peak. The further anterior one comes with the hairline, the more anterior must come with the temporal peak restoration and vice-versa.

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