title: Tenascin C protects aorta from acute dissection in mice.
abstract: Acute aortic dissection (AAD) is caused by the disruption of intimomedial layer of the aortic walls, which is immediately life-threatening. Although recent studies indicate the importance of proinflammatory response in pathogenesis of AAD, the mechanism to keep the destructive inflammatory response in check is unknown. Here, we report that induction of tenascin-C (TNC) is a stress-evoked protective mechanism against the acute hemodynamic and humoral stress in aorta. Periaortic application of CaCl₂ caused stiffening of abdominal aorta, which augmented the hemodynamic stress and TNC induction in suprarenal aorta by angiotensin II infusion. Deletion of Tnc gene rendered mice susceptible to AAD development upon the aortic stress, which was accompanied by impaired TGFβ signaling, insufficient induction of extracellular matrix proteins and exaggerated proinflammatory response. Thus, TNC works as a stress-evoked molecular damper to maintain the aortic integrity under the acute stress.
authors: 1] Department of Molecular Cardiovascular Biology, Yamaguchi University School of Medicine [2] Division of Cardiology, Department of Medicine and Clinical Science, Yamaguchi University Graduate School of Medicine [3] Division of Cardiovascular Medicine, Medical Science for Control of Pathological Processes, Graduate School of Comprehensive Human Science, University of Tsukuba.
authors: Taizo
authors: T
authors: Kimura
authors: Division of Cardiology, Department of Medicine and Clinical Science, Yamaguchi University Graduate School of Medicine.
authors: Kozoh
authors: K
authors: Shiraishi
authors: Cardiovascular Research Institute, Kurume University.
authors: Aya
authors: A
authors: Furusho
authors: Cardiovascular Research Institute, Kurume University.
authors: Sohei
authors: S
authors: Ito
authors: Cardiovascular Research Institute, Kurume University.
authors: Saki
authors: S
authors: Hirakata
authors: Cardiovascular Research Institute, Kurume University.
authors: Norifumi
authors: N
authors: Nishida
authors: 1] Department of Molecular Cardiovascular Biology, Yamaguchi University School of Medicine [2] Department of Surgery and Clinical Science, Yamaguchi University Graduate School of Medicine.
authors: Koichi
authors: K
authors: Yoshimura
authors: 1] Department of Pathology and Matrix Biology, Mie University Graduate School of Medicine [2] Mie University Research Center for Matrix Biology, Mie University Graduate School of Medicine.
authors: Kyoko
authors: K
authors: Imanaka-Yoshida
authors: 1] Department of Pathology and Matrix Biology, Mie University Graduate School of Medicine [2] Mie University Research Center for Matrix Biology, Mie University Graduate School of Medicine.
authors: Toshimichi
authors: T
authors: Yoshida
authors: 1] Department of Molecular Cardiovascular Biology, Yamaguchi University School of Medicine [2] Division of Cardiology, Department of Medicine and Clinical Science, Yamaguchi University Graduate School of Medicine.
authors: Yasuhiro
authors: Y
authors: Ikeda
authors: Cardiovascular Research Institute, Kurume University.
authors: Takanobu
authors: T
authors: Miyamoto
authors: Cardiovascular Research Institute, Kurume University.
authors: Takafumi
authors: T
authors: Ueno
authors: Department of Surgery and Clinical Science, Yamaguchi University Graduate School of Medicine.
authors: Kimikazu
authors: K
authors: Hamano
authors: National Center for Global Health and Medicine, Tokyo, Japan.
authors: Michiaki
authors: M
authors: Hiroe
authors: Division of Cardiovascular Medicine, Medical Science for Control of Pathological Processes, Graduate School of Comprehensive Human Science, University of Tsukuba.
authors: Kazutaka
authors: K
authors: Aonuma
authors: 1] Department of Molecular Cardiovascular Biology, Yamaguchi University School of Medicine [2] Division of Cardiology, Department of Medicine and Clinical Science, Yamaguchi University Graduate School of Medicine.
authors: Masunori
authors: M
authors: Matsuzaki
authors: Cardiovascular Research Institute, Kurume University.
authors: Tsutomu
authors: T
authors: Imaizumi
authors: 1] Department of Molecular Cardiovascular Biology, Yamaguchi University School of Medicine [2] Cardiovascular Research Institute, Kurume University.
authors: Hiroki
authors: H
authors: Aoki
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D001014:Aortic Aneurysm / Q000378:metabolism / Q000473:pathology; D002122:Calcium Chloride / Q000494:pharmacology; D002478:Cells, Cultured; D004195:Disease Models, Animal; D020869:Gene Expression Profiling; D006439:Hemodynamics / Q000187:drug effects; D051379:Mice; D018345:Mice, Knockout; D032389:Myocytes, Smooth Muscle / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D019063:Tenascin / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D016212:Transforming Growth Factor beta / Q000378:metabolism
chemical_list: D019063:Tenascin; D016212:Transforming Growth Factor beta; D000804:Angiotensin II; D002122:Calcium Chloride