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Investigation of the expression of the extracellular matrix glycoproteins tenascin and fibronectin during acne vulgaris
Authors:HE KNAGGS  AM LAYTON  C MORRIS  EJ WOOD  UB HOLLAND  WJ CUNLIFFH
Institution:Department of Dermatology, The General Infirmary at Leeds, Great George Street, U-eds LSI 3EX, U.K.;Department of Biochemistry and Molecular Biology, University of Leeds, Leeds LS2 9JT, U.K.
Abstract:Summary Tenascin and fibronectin are extracellular matrix glycoproteins which can interact with cells and alter their capacity to adhere, migrate and proliferate. In contrast with fibronectin, tenascin has a restricted distribution in normal skin, but is induced during epidermal proliferation, and in wound healing. Because acne involves hyperproliferation of ductal keratinocytes, and rupture of the duct may occur during inflammation, the distribution of tenascin and fibronectin was investigated in acne lesions, and also in acne keloids. Biopsies obtained from patients a ending the acne clinics were cryostat-sectioned and stained with tenascin antiserum. The extent of tenascin staining in the dermis around the pilosebaceous unit was measured. Tenascin was continually expressed around normal control pilosebaceous ducts: it was maximal around the acroinfundibulum, extending 20·83±9·32 μm n = 14) into the dermis, compared with staining around the infrainfundibulum (11·88± 3·70 μm. N = 14). This was not significantly different from staining around normal pilosebaceous ducts obtained from acne patients. In non-inflamed lesions tenascin staining increased significantly around the infrainfundibulum to 76·88±29·97 μm ( n = 12), compared with this region in the normal follicles. The staining around the acroinfundibulum did not change significantly. Around inflamed lesions the whole of the dermis was positive for tenascin. No changes were detected in the staining pattern for fibronectin, which stained the whole dermis in all the sections tested. The keloid samples stained strongly for both extracellular matrix glycoproteins. Thus, increased tenascin expression appears to be associated with the development of acne lesions. Tenascin production may be induced by hyperproliferation of ductal keratinocytes and localized loss of control in this process may contribute to the production of acne keloids.
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