Expression of tenascin, biglycan and decorin in disorders of keratinization

Abstract

The distribution of three (recently discovered) extracellular matrix components (tenascin, biglycan and decorin) was studied in normal adult human skin and in a number of monogenic disorders of keratinization, using immunohistology. The expression of tenascin, which is sparsely distributed in normal human dermis, was found to be grossly increased in epidermolytic hyperkeratoses and in Darier's disease. Tenascin expression in three types of ichthyosis (X-linked recessive ichthyosis, autosomal dominant ichthyosis vulgaris, non-erythrodermic lamellar ichthyosis) was similar to that of normal skin. The presence of biglycan and decorin did not show a marked variation between the different disorders studied, suggesting that their expression is subject to regulatory mechanisms distinct from those of tenascin. The increased expression of tenascin in two disorders of keratinization with a hyperproliferative phenotype, lends further support to the hypothesis that dermal tenascin expression is increased as a result of epidermal hyperproliferation.

Deficiency of Tenascin-X Causes Abnormalities in Dermal Elastic Fiber Morphology

“…Sections were blocked with 20% normal goat serum or 20% normal swine serum (Vector Laboratories Inc., Burlingham, California) before application of primary antibodies. Sections were subsequently labeled with primary antibodies: monoclonal antielastin (BA-4, Sigma), monoclonal anti-fibrillin-1 (MAB2502; Chemicon, Temecula, California), or anti-decorin (Steijlen et al, 1994). Then, sections were washed and incubated with biotinylated secondary antibody followed by a complex of avidine and biotinylated horseradish peroxidase according to the manufacturer's instructions (Vector Labs).…”

Coordinate upregulation of tenascin C expression with degree of photodamage in human skin

“…The biopsies were taken from the volar forearm (photodamaged) and the inner upper arm (sunprotected). Using a 10-point scale, the extent of photodamage was clinically assessed as absent (0), mild (1), low moderate (2, 3), moderate (4,5), high moderate (6,7) or severe (8,9), based on the photodamage characteristics of fine lines, mottled pigmentation, sallowness and an overall assessment with reference to standard photographs. The 10-point photodamage scale used is based on the photonumeric scale described by Griffiths et al 16 adapted for arm sites, has been validated in-house by extensive comparison of gross and histological evidence of photodamage, and has been used extensively for several years.…”

“…Tenascin expression and isoform patterns are spatially and temporally regulated during tightly controlled tissue remodelling processes, including embryogenetic and morphogenetic development, and wound healing 1 –4 . Tenascin is elevated in the dermis in many hyperproliferative skin diseases and neoplasias, such as psoriasis, basal cell carcinoma, Darier's disease, Bowen's disease and solar keratosis, where physiological processes might be considered to be ‘uncontrolled’ 5 –7 …”

“…[1][2][3][4] Tenascin is elevated in the dermis in many hyperproliferative skin diseases and neoplasias, such as psoriasis, basal cell carcinoma, Darier's disease, Bowen's disease and solar keratosis, where physiological processes might be considered to be 'uncontrolled'. [5][6][7] In normal adult skin, tenascin and its large isoform are reported as sparsely, often discontinuously distributed in the upper papillary dermis adjacent to the dermoepidermal junction; tenascin is also localized to capillary basement membranes and regions of morphogenetic flux such as the hair follicles. 8 During cutaneous wound repair, tenascin expression increases rapidly and dramatically (by 1 day postinsult), becoming continuous along the wound edge, and appearing in a diffuse pattern throughout the granulation matrix.…”