Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, the distribution of tenascin immunoreactivity in 44 cases of vulvar lichen sclerosus (LS) was investigated. To assess the epithelial basement membrane structure, immunostaining with an antibody to type IV collagen was performed. Ten selected cases were also analyzed by in situ hybridization with a tenascin RNA probe to study the cellular distribution of tenascin mRNA synthesis in LS. Strong tenascin immunoreactivity could be found in LS, especially in areas with subepithelial edema and marked inflammation. By in situ hybridization, signals for tenascin mRNA could be found in basal keratinocytes, dermal fibroblasts, and endothelial cells. Staining for type IV collagen often revealed attenuation and discontinuity in the basement membrane. The abnormal accumulation of tenascin in LS suggests that it may participate in the pathogenesis of this disease. As shown by in situ hybridization, the cell types responsible for tenascin synthesis are basal keratinocytes, dermal fibroblasts, and endothelial cells. Because tenascin, together with fibronectin, is able to upregulate the expression of 92 kDa collagenase and stromelysin in fibroblasts, the matrix destruction and basement membrane damage in LS may partly be a consequence of an abnormal accumulation and synthesis of tenascin. The upregulation of tenascin synthesis in dermal fibroblasts, endothelial cells, and keratinocytes in LS could be mediated by an abnormal expression of growth factors, most notably TGF-beta, which are able to stimulate tenascin synthesis in many non-neoplastic and neoplastic cell lines.
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PMID:Tenascin expression in lichen sclerosus. 942 Oct 69

Lichen sclerosus et atrophicus (LSA) is a chronic inflammatory skin disease characterized by white porcelain-like sclerotic skin lesions. It is most commonly seen in adult females and usually affects the genitoanal area. Extragenital LSA appears in 15-20% of cases. We report a 9-year-old Caucasian girl suffering from extragenital LSA that was resistant to conventional treatment. After 40 treatment sessions with low-dose UVA1 phototherapy, all skin lesions were resolved completely. Moreover, the improvement of skin status has been sustained during 6-months of follow-up. Long-wave UVA irradiation has been shown to induce intensively collagenase activity in human dermal fibroblasts. We suggest that UVA1 irradiation could be an effective treatment in patients suffering from extragenital LSA.
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PMID:Low-dose ultraviolet-A1 phototherapy for lichen sclerosus et atrophicus. 1126 Jan 73