1998 Fiscal Year Final Research Report Summary
Differential effects of dominant negative mutants of desmoglein, desmocollin, and E-cadherin on cell-cell adhesion of keratinocytes.
| Project/Area Number |
09670883
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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 | Ehime University |
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Principal Investigator |
SAYAMA Koji EHIME UNIVERSITY,UNIVERSITYHOSPITAL,ASSISTANT PROFESSOR, 医学部附属病院, 講師 (80187286)
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| Project Period (FY) |
1997 – 1998
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| Keywords | Keratinocytes / Adenovirus Vector / Cre / loxP / Desmoglein-3 / Desmocollin-3 / Cadherin / Desmosome / Adherens junction |
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| Research Abstract |
Epithelial cell-cell adhesion is considered to be important in development and maintenance of tissue integrity of stratified squamous epithelium. The purpose of this study is to investigate the roles of classic and desmosomal cadherins in the maintenance of keratinocyte cell-cell adhesion. With adenovirus vector (Ad), we studied the effect of mutants of E-cadherin, desmoglein 3 , desmocollin3 which were constructed by deleting a large part of the extracellular domain (E-cadDELTA EC,Dsg3DELTA EC, Dsc3DELTA EC) on HaCaT cell. First, we tried to make Ad that directly express the mutant. But due to the toxicity or other unknown mechanism, we could not make Ad. Then we used Ad Cre-loxP system. LoxP flanked mutant vector does not express itself, but co-infection of AdCre switches on the mutant transcription. Under high calcium condition, Dsg3DELTAEC expression disrupted only desmosome, Dsc3DELTA ECor E-cadDELTAEC expression disrupted desmosome and also adherens junction in inimunofluorescence staining. By 2h after calcium elevation, all the mutants inhibited desmosome formation. But only Dsg3DELTAEc could not inhibit adherens junction formation. These results suggest that desmoglein and desniocollin may play a different role in cell-cell adhesion.
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