TY - JOUR
T1 - Involvement of urokinase-type plasminogen activator in acantholysis induced by pemphigus IgG
AU - Morioka, Shinji
AU - Lazarus, Gerald S.
AU - Jensen, Pamela J.
N1 - Funding Information:
Manuscript received January 20, 1987; accepted for publication April 9, 1987. This work was supported by National In stitutes of Hea lth grants 5 ROJ AM 32069 and 2 ROJ AM 32070. Reprint requests to: Dr. P. J. Jensen, D epartment of Derm atology, 330 Medica l Ed uca ti on Building, 36th & Hami lton Walk, University of Pennsylvania, Philadelphia, PA 19104 * A preliminary report of this work was presented at the national meeting of the Society for Investigative Dermatology, May 1984. tPrcsent address: Department of Dermatology, Juntendo University, School of Medicine, Tokyo, Japan. Abbreviations: DME: Dulbecco's modified Eagle's medium PAc plasminogen activator
PY - 1987/11
Y1 - 1987/11
N2 - Pemphigus IgG induces acantholysis in skin organ culture without the involvement of complement. Urokinase-type plasminogen activator, a proteolytic enzyme, has been implicated in the development of acantholysis. To test this hypothesis, we prepared a rabbit anti-urokinase antibody, which inhibited the plasminogen activator activity in normal human epidermis and in cultured keratinocytes. When added to skin organ cultures along with pemphigus IgG, anti-urokinase IgG completely prevented the development of acantholysis. Normal or preimmune rabbit IgG had no effect on pemphigus IgG-induced acantholysis. Plasminogen activator converts the zymogen plasminogen to its active form plasmin, a broad specificity serine proteinase. When high concentrations of plasminogen alone were added to skin organ culture, acantholysis of the pemphigus foliaceous type was induced. Anti-urokinase antibody also inhibited plasminogen-induced acantholysis. These results strongly support a pivotal role for plasminogen activator in the development of acantholysis.
AB - Pemphigus IgG induces acantholysis in skin organ culture without the involvement of complement. Urokinase-type plasminogen activator, a proteolytic enzyme, has been implicated in the development of acantholysis. To test this hypothesis, we prepared a rabbit anti-urokinase antibody, which inhibited the plasminogen activator activity in normal human epidermis and in cultured keratinocytes. When added to skin organ cultures along with pemphigus IgG, anti-urokinase IgG completely prevented the development of acantholysis. Normal or preimmune rabbit IgG had no effect on pemphigus IgG-induced acantholysis. Plasminogen activator converts the zymogen plasminogen to its active form plasmin, a broad specificity serine proteinase. When high concentrations of plasminogen alone were added to skin organ culture, acantholysis of the pemphigus foliaceous type was induced. Anti-urokinase antibody also inhibited plasminogen-induced acantholysis. These results strongly support a pivotal role for plasminogen activator in the development of acantholysis.
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U2 - 10.1111/1523-1747.ep12460937
DO - 10.1111/1523-1747.ep12460937
M3 - Article
C2 - 3117905
AN - SCOPUS:0023233253
SN - 0022-202X
VL - 89
SP - 474
EP - 477
JO - Journal of Investigative Dermatology
JF - Journal of Investigative Dermatology
IS - 5
ER -