NDLI: Expression of adhesion molecule T-cadherin is increased during neointima formation in experimental restenosis

Content Provider	Springer Nature Link
Author	Kudrjashova, Elena Bashtrikov, Pavel Bochkov, Valery Parfyova, Yelena Tkachuk, Vsevolod Antropova, Julia Iljinskaya, Olga Tararak, Eduard Erne, Paul Ivav, Danila Philippova, Maria Resink, Therese J.
Copyright Year	2002
Abstract	Phenotypic modulation, migration and proliferation of vascular smooth muscle cells (SMCs) are major events in restenosis after percutaneous transluminal angioplasty. Surface cell adhesion molecules, essential to morphogenesis and maintenance of adult tissue architecture, are likely to be involved, but little is known about cell adhesion molecules expressed on SMCs. T-cadherin is a glycosyl phosphatidylinositol-anchored member of the cadherin superfamily of adhesion molecules. Although highly expressed in vascular and cardiac tissues, its function in these tissues is unknown. We previously reported increased expression of T-cadherin in intimal SMCs in atherosclerotic lesions and proposed a role for T-cadherin in phenotype control. Here we performed immunohistochemical analysis of spatial and temporal changes in vascular T-cadherin expression following balloon catheterisation of the rat carotid artery. T-cadherin expression in SMCs markedly increases in the media early (1–4 days) after injury, and later (day 7–28) in forming neointima, especially in its preluminal area. Staining for monocyte/macrophage antigen ED-1, proliferating cell nuclear antigen and smooth muscle alpha-actin revealed that spatial and temporal changes in T-cadherin level coincided with the peak in cell migration and proliferation activity during neointima formation. In colchicine-treated cultures of rat aortic SMCs T-cadherin expression is increased in dividing M-phase cells but decreased in non-dividing cells. Together the data support an association between T-cadherin expression and SMC phenotype.
Starting Page	281
Ending Page	290
Page Count	10
File Format	PDF
ISSN	09486143
Journal	Histochemistry and Cell Biology
Volume Number	118
Issue Number	4
e-ISSN	1432119X
Language	English
Publisher	Springer-Verlag
Publisher Date	2002-09-27
Publisher Place	Berlin/Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Cell Biology Histology Molecular Biology Medical Laboratory Technology

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