Abstract

The morphology of the skin of the mutant hairless USP mouse was studied by histological, histochemical and immunohistochemical methods and compared to the skin of BALB/c mice. Representative sections of the dorsal skin from mice of both strains aged 18 days, and 1, 3, 6, and 8 months were studied. Sections stained with hematoxylin and eosin showed cystic formations called utricles and dermal cysts in the dermis that increased in size and number during growth. Skin thickness increased significantly at 8 months. Sections stained with picrosirius and examined with polarized light, displayed different colors, suggesting different thicknesses of dermal collagen fibers (probably types I and III). Weigert, Verhoeff and resorcin-fuchsin stains revealed fibers of the elastic system. The PAS and Alcian blue methods revealed neutral and acid glycosaminoglycans in the skin ground substance of both mouse strains. Immunohistochemical staining for fibronectin and laminin did not show differences between the mutant and BALB/c mice. Mast cells stained by the Gomori method and macrophages positive for HAM 56 antibodies were observed in both mouse strains. Except for the presence of enlarged cysts in the hairless strain, no qualitative differences were found during development of the skin of BALB/c and the mutant hairless mice.

Highlights

  • The hairless and rhino mutants are the most intensively studied models of hair cycle defects

  • After the first hair cycle, hair is lost over the whole body at the same time and the loss progresses until the mice are fully naked (3)

  • We describe the kinetics of the development of the skin lesions in hairless USP (hrUSP) mutant mice

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Summary

Introduction

The hairless and rhino mutants are the most intensively studied models of hair cycle defects. Affected mice lose their hair progressively from the head to the tail at the end of the first hair cycle because the second hair cycle is defective (1). From the hairless mice described earlier, this mutant does not show a defined pattern of hair loss. To determine if the hrUSP and rhino mutants might be alleles of the same gene, heterozygous mice of both strains were mated. Fifty percent of hrUSP/+ and rhino/+ offspring showed the hairless phenotype, indicating that the two mutations do not complement each other in vivo, being alleles of a single gene

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