1996 Fiscal Year Final Research Report Summary
Signal Transduction Induced by Desmosomal Cadherin Antigen-Antibody Reaction in Bullous Formation in Pemphigus
| Project/Area Number |
07670938
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Gifu University |
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Principal Investigator |
SEISHIMA Mariko Gifu University School of Medicine, Department of Dermatology, Assistant Professor, 医学部・附属病院, 講師 (00171314)
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| Project Period (FY) |
1995 – 1996
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| Keywords | Pemphigus / Acantholysis / Desmosome / Intracellular Calcium / Phospholipase C / Plasminogen Activator / Signal Transduction / Protein Kinase C |
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| Research Abstract |
Pemphigus vulgaris (PV) is an autoimmune skin disease characterized by the autoantibodies against desmoglein 3. Although the exact mechanism for cutaneus blistering induced by PV-IgG binding to keratinocytes has not yet elucidated, pemphigus IgG-induced acantholysis may be caused by proteinases from keratinocytes such as plasminogen activator. We have studied the effects of PV-IgG on the intracellular signal transduction events, and demonstrated that PV-IgG-binding to DJM-1 cells (a squamous cell carcinoma line) induces a transient increase in phospholipase C activation, and an increased inositol 1,4,5-trisphophate production, with a concomitant increase in intracellular calcium concentration. These events are directly associated with secretion of plasminogen activator into the culture medium, and subsequent cell-cell detachment.
In addition, the protein kinase C (PKC) activity in the particulate/cytoskeleton fraction was increased following PV-IgG exposure, peaking at 1 min, and being sustained for at leaset 30 min. These findings suggest that an activation profile of PKC may be involvedin mediationg the intracellular signaling events induced by PV-IgG binding to desmoglein 3 in cultured human keratinocytes.
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Research Products
(12 results)
