title: Tenascin-C is expressed in abdominal aortic aneurysm tissue with an active degradation process.
abstract: Abdominal aortic aneurysm (AAA) is a common disease caused by segmental weakening of the aortic walls and progressive aortic dilation leading to the eventual rupture of the aorta. Currently no biomarkers have been established to indicate the disease status of AAA. Tenascin-C (TN-C) is a matricellular protein that is synthesized under pathological conditions. In the current study, we related TN-C expression to the clinical course and the histopathology of AAA to investigate whether the pattern of TN-C expression could indicate the status of AAA. We found that TN-C and matrix metalloproteinase (MMP)-9 were highly expressed in human AAA. In individual human AAA TN-C deposition associated with the tissue destruction, overlapped mainly with the smooth muscle actin-positive cells, and showed a pattern distinct from macrophages and MMP-9. In the mouse model of AAA high TN-C expression was associated with rapid expansion of the AAA diameter. Histological analysis revealed that TN-C was produced mainly by vascular smooth muscle cells and was deposited in the medial layer of the aorta during tissue inflammation and excessive destructive activities. Our findings suggest that TN-C may be a useful biomarker for indicating the pathological status of smooth muscle cells and interstitial cells in AAA.
authors.affiliation: Department of Molecular Cardiovascular Biology, Yamaguchi University School of Medicine, Kurume, Japan.
authors.forename: Taizo
authors.initials: T
authors.lastname: Kimura
authors.forename: Koichi
authors.initials: K
authors.lastname: Yoshimura
authors.forename: Hiroki
authors.initials: H
authors.lastname: Aoki
authors.forename: Kyoko
authors.initials: K
authors.lastname: Imanaka-Yoshida
authors.forename: Toshimichi
authors.initials: T
authors.lastname: Yoshida
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Ikeda
authors.forename: Noriyasu
authors.initials: N
authors.lastname: Morikage
authors.forename: Hisako
authors.initials: H
authors.lastname: Endo
authors.forename: Kimikazu
authors.initials: K
authors.lastname: Hamano
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Imaizumi
authors.forename: Michiaki
authors.initials: M
authors.lastname: Hiroe
authors.forename: Kazutaka
authors.initials: K
authors.lastname: Aonuma
authors.forename: Masunori
authors.initials: M
authors.lastname: Matsuzaki
mesh_terms: D000818:Animals; D001012:Aorta, Abdominal / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D017544:Aortic Aneurysm, Abdominal / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D015415:Biomarkers / Q000378:metabolism; D002122:Calcium Chloride / Q000633:toxicity; D004195:Disease Models, Animal; D006801:Humans; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D051379:Mice; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology; D019063:Tenascin / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D019063:Tenascin; D020780:Matrix Metalloproteinase 9; D002122:Calcium Chloride