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Open Access Green as soon as Postprint is submitted to ZB.
Talin and vinculin are downregulated in atherosclerotic plaque; Tampere Vascular Study.
Atherosclerosis 255, 43-53 (2016)
Background and aims Focal adhesions (FA) play an important role in the tissue remodeling and in the maintenance of tissue integrity and homeostasis. Talin and vinculin proteins are among the major constituents of FAs contributing to cellular well-being and intercellular communication. Methods Microarray analysis (MA) and qRT-PCR low-density array were implemented to analyze talin-1, talin-2, meta-vinculin and vinculin gene expression in circulating blood and arterial plaque. Results All analyzed genes were significantly and consistently downregulated in plaques (carotid, abdominal aortic and femoral regions) compared to left internal thoracic artery (LITA) control. The use of LITA samples as controls for arterial plaque samples was validated using immunohistochemistry by comparing LITA samples with healthy arterial samples from a cadaver. Even though the differences in expression levels between stable and unstable plaques were not statistically significant, we observed further negative tendency in the expression in unstable atherosclerotic plaques. The confocal tissue imaging revealed gradient of talin-1 expression in plaque with reduction close to the vessel lumen. Similar gradient was observed for talin-2 expression in LITA controls but was not detected in plaques. This suggests that impaired tissue mechanostability affects the tissue remodeling and healing capabilities leading to development of unstable plaques. Conclusions The central role of talin and vinculin in cell adhesions suggests that the disintegration of the tissue in atherosclerosis could be partially driven by downregulation of these genes, leading to loosening of cell-ECM interactions and remodeling of the tissue.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Atherosclerosis ; Focal Adhesion ; Mechanobiology ; Talin ; Vinculin; Actin-binding; Shear-stress; Adhesion; Expression; Protein; Cell; Domain; Mechanotransduction; Macrophages; Endothelium
ISSN (print) / ISBN
0021-9150
e-ISSN
1879-1484
Journal
Atherosclerosis
Quellenangaben
Volume: 255,
Pages: 43-53
Publisher
Elsevier
Publishing Place
Amsterdam
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Epidemiology II (EPI2)