An immunohistochemical study of the distribution of plasminogen and plasminogen activators in bullous pemphigoid

VA Venning, F Wojnarowska… - Clinical and …, 1993 - Wiley Online Library
VA Venning, F Wojnarowska, S Cederholm‐Williams
Clinical and experimental dermatology, 1993Wiley Online Library
Abnormalities of the cutaneous plasminogen/plasminogen activator system have been
associated with acantholytic disorders, psoriasis, keratinocytes in culture, and epidermis in
healing wounds. The present study was undertaken to investigate the possible role of the
plasmin/plasminogen protease system in lesion development in bullous pemphigoid (BP).
Using polyclonal antibodies and a fluorescent technique, the immunohistochemical
distribution of plasmin/plasminogen, fibrinogen and the plasminogen activators, urokinase …
Summary
Abnormalities of the cutaneous plasminogen/plasminogen activator system have been associated with acantholytic disorders, psoriasis, keratinocytes in culture, and epidermis in healing wounds. The present study was undertaken to investigate the possible role of the plasmin/plasminogen protease system in lesion development in bullous pemphigoid (BP). Using polyclonal antibodies and a fluorescent technique, the immunohistochemical distribution of plasmin/plasminogen, fibrinogen and the plasminogen activators, urokinase (uPA) and tissue plasminogen activator (tPA), were studied in lesional and non‐fesional skin from nine BP patients, one with linear IgA disease (LAD) and one with pemphigoid gestationis (PG). The distribution of the proteases was compared with that in normal skin (n=4) and in suction blisters (n=2).
In normal skin, fibrinogen, tPA and uPA were absent from the epidermis and plasminogen was confined to the basal layer. Uninvolved BP skin was identical to controls. Focal areas of suprabasal plasminogen expression in the region of a blister was seen in 3/9 BP lesions and in 1/2 suction blisters. In 6/9 BP lesions and both uninvolved and lesional LAD and PG skin were identical to controls, and no suprabasal expression of plasminogen was present.
These findings suggest that suprabasal plasminogen expression is unlikely to play a fundamental role in the pathogenesis of blister formation in BP as enhanced expression was not present in every case and the finding was not specific to BP, also occurring in a suction blister. Enhanced plasminogen expression rather may be a reflection of the processes of tissue repair.
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