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氨基脲敏感胺氧化酶基因敲除小鼠的颈动脉僵硬度、弹性纤维网络与血管反应性

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

作者信息

Mercier Nathalie, Osborne-Pellegrin Mary, El Hadri Khadija, Kakou Augustine, Labat Carlos, Loufrani Laurent, Henrion Daniel, Challande Pascal, Jalkanen Sirpa, Fève Bruno, Lacolley Patrick

机构信息

INSERM U684, Vandoeuvre-les-Nancy, France.

出版信息

Cardiovasc Res. 2006 Nov 1;72(2):349-57. doi: 10.1016/j.cardiores.2006.08.008. Epub 2006 Aug 17.

Abstract

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.

摘要

目的

我们使用包括高分辨率回声跟踪在内的各种技术,研究了氨基脲敏感胺氧化酶基因敲除小鼠(SSAO -/-)的动脉表型。

方法与结果

SSAO -/-小鼠在麻醉状态下动脉血压无变化。仅在颈动脉(CA)测量的体内动脉直径,SSAO -/-小鼠高于SSAO +/+小鼠。SSAO -/-和 +/+小鼠之间的弹性模量-壁应力曲线和CA破裂压力相似,表明动脉壁硬度或机械强度无变化。两种基因型之间的不溶性弹性蛋白、总胶原蛋白含量和弹性层形态无显著差异。在SSAO -/-小鼠的主动脉环和肠系膜动脉中未观察到血管反应性的改变。主动脉赖氨酰氧化酶(LO)活性保持不变,表明SSAO缺失并未伴随LO活性的代偿性增加。

结论

这是首次对缺乏SSAO的动脉进行的功能研究。我们的结果表明,SSAO -/-小鼠的动脉直径增加,同时动脉力学性能正常,提示SSAO缺乏可能有助于动脉壁重塑。然而,这些结果与SSAO参与弹性纤维组织、弹性蛋白交联过程和血管反应性的假设相悖。

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