von Willebrand factor deficiency does not influence angiotensin II-induced abdominal aortic aneurysm formation in mice.
von Willebrand factor deficiency does not influence angiotensin II-induced abdominal aortic aneurysm formation in mice.
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DOI：
10.1038/s41598-018-35029-8
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发表时间：
2018-11-09
影响因子：
4.6
通讯作者：
De Meyer SF
中科院分区：
文献类型：
--
作者：
Portier I;Martinod K;Desender L;Vandeputte N;Deckmyn H;Vanhoorelbeke K;De Meyer SF
腹主动脉瘤（AAA）是指腹主动脉的局部扩张超过正常直径50%。AAA病理生理学的特征在于进行性炎症、血管壁不稳定和血栓形成。我们的目的是研究血管性血友病因子（VWF），血栓炎性血浆蛋白，在AAA病理生理学使用解剖为基础的和血管紧张素II输注诱导的AAA小鼠模型的潜在参与。通过皮下植入渗透泵，连续释放1000 ng/kg/min血管紧张素II，在野生型和VWF缺陷小鼠中诱导AAA形成。监测存活率，但两组之间未观察到显著差异。28天后，收获存活小鼠的肾上腺主动脉段。AAA的发病率和严重程度在野生型和VWF缺陷型小鼠中相似，表明AAA的形成不受VWF缺乏的显著影响。尽管VWF血浆水平在输注期后升高，但这些升高与AAA进展无关。此外，对AAA重要标志（包括弹性降解、壁内血栓形成和白细胞浸润）的详细组织学分析并未显示两组之间存在差异。这些数据表明，至少在血管紧张素II输注诱导的AAA小鼠模型中，VWF在AAA病理生理学中的作用是有限的。
Abdominal aortic aneurysm (AAA) refers to a localized dilation of the abdominal aorta that exceeds the normal diameter by 50%. AAA pathophysiology is characterized by progressive inflammation, vessel wall destabilization and thrombus formation. Our aim was to investigate the potential involvement of von Willebrand factor (VWF), a thrombo-inflammatory plasma protein, in AAA pathophysiology using a dissection-based and angiotensin II infusion-induced AAA mouse model. AAA formation was induced in both wild-type and VWF-deficient mice by subcutaneous implantation of an osmotic pump, continuously releasing 1000 ng/kg/min angiotensin II. Survival was monitored, but no significant difference was observed between both groups. After 28 days, the suprarenal aortic segment of the surviving mice was harvested. Both AAA incidence and severity were similar in wild-type and VWF-deficient mice, indicating that AAA formation was not significantly influenced by the absence of VWF. Although VWF plasma levels increased after the infusion period, these increases were not correlated with AAA progression. Also detailed histological analyses of important AAA hallmarks, including elastic degradation, intramural thrombus formation and leukocyte infiltration, did not reveal differences between both groups. These data suggest that, at least in the angiotensin II infusion-induced AAA mouse model, the role of VWF in AAA pathophysiology is limited.
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DOI：
10.1016/j.ejvs.2010.09.011
发表时间：
2011-01-01
影响因子：
5.7
作者：
Moll, F. L.;Powell, J. T.;Rica, J-B
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影响因子：
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作者：
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影响因子：
5.9
作者：
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影响因子：
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