Carotid arterial stiffness, elastic fibre network and vasoreactivity in semicarbazide-sensitive amine-oxidase null mouse

被引:34
作者
Mercier, Nathalie
Osborne-Pellegrin, Mary
El Hadri, Khadija
Kakou, Augustine
Labat, Carlos
Loufrani, Laurent
Henrion, Daniel
Challande, Pascal
Jalkanen, Sirpa
Feve, Bruno
Lacolley, Patrick
机构
[1] Fac Med Vandoeuvre Nancy, U684, INSERM, F-54505 Vandoeuvre Les Nancy, France
[2] Turku Univ, MediCity Res Lab, FIN-20520 Turku, Finland
[3] Natl Publ Hlth Inst, Turku, Finland
[4] INSERM, U698, Paris, France
[5] CNRS, UMR 7079, Paris, France
[6] CNRS, UMR 6188, Angers, France
[7] Univ Paris 06, FRE 2867, St Cyr Lecole, France
[8] INSERM, U693, F-94275 Le Kremlin Bicetre, France
关键词
amine oxidase; arterial stiffness; elastin; gene invalidation; SSAO; vascular smooth muscle cells;
D O I
10.1016/j.cardiores.2006.08.008
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: We examined the arterial phenotype of semicarbazide-sensitive amine-oxidase null mouse (SSAO -/-) using various techniques including high resolution echotracking. Methods and results: SSAO -/- mice showed no change in arterial pressure under anesthesia. The in vivo arterial diameter, only measured in the carotid artery (CA), was higher in SSAO -/- than in SSAO +/+ animals. Elastic modulus-wall stress curves and CA rupture pressure were similar between SSAO -/- and +/+ mice, indicating no change in arterial wall stiffness or mechanical strength. There was no significant difference in insoluble elastin, total collagen content and elastic lamellar morphology between the two genotypes. No alteration in vascular reactivity was observed in aortic rings and mesenteric arteries from SSAO -/- mice. Aortic lysyl oxidase (LO) activity remained unaltered, indicating that SSAO invalidation is not accompanied by a compensatory increase in LO activity. Conclusion: This is the first functional study of arteries lacking SSAO. Our results indicate that SSAO -/- mice present an increased arterial diameter associated with normal arterial mechanical properties, suggesting that SSAO deficiency might contribute to arterial wall remodeling. However, these results argue against the hypothesis that SSAO intervenes in elastic fibre organization, elastin cross-linking processes and vasoreactivity. (c) 2006 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:349 / 357
页数:9
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