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基质金属蛋白酶-8 和 -15 与升主动脉夹层易感性的关系。

A disintegrin and metalloprotease -8 and -15 and susceptibility for ascending aortic dissection.

机构信息

Department of Clinical Chemistry, Medical School, Tampere University Hospital and Tampere University, Finland.

出版信息

Scand J Clin Lab Invest. 2011 Oct;71(6):515-22. doi: 10.3109/00365513.2011.591939. Epub 2011 Jul 6.

DOI:10.3109/00365513.2011.591939
PMID:21728902
Abstract

BACKGROUND. Dilatation of the ascending aorta (AA) is affected by extra-cellular matrix modifications and inflammation. A disintegrin and metalloproteases (ADAMs) may reveal differences between AA and ascending aortic dissection (AD). We characterized the inflammatory histology of AD and AA and examined the role of ADAM8 and -15 in these diseases. MATERIAL AND METHODS. Aortic wall histology and immunohistochemistry for leukocytes, T- and B-lymphocytes, plasma cells, macrophages, endothelial cells, smooth muscle cells, cell proliferation, elastase and Van-Gieson-staining were performed to 40 consecutive patients that underwent surgery for AA or AD. The expressions of ADAM8 and -15 mRNA and proteins were evaluated using QRT-PCR and immunohistochemistry. RESULTS. Thirty-four patients were enrolled, of which 29 had AA and five had AD of the ascending aorta. B-cells throughout the aortic wall and intimal plasma cells were more numerous during AD as compared with AA (p < 0.05). The gene expressions for ADAM8 and -15 were notably lower in AA as compared with AD. The median for down-regulation of ADAM8 and -15 in AA was -2.7 and -1.8, respectively. ADAM8 and -15 were mainly found in the media layer in patients with AD. Two of the patients with AA and increased ADAMs developed AD of the remaining aorta. CONCLUSIONS. The involvement of ADAM8 and -15 together with inflammation consisting of B-cells may indicate active remodelling of the aortic wall leading to AD.

摘要

背景

升主动脉(AA)的扩张受细胞外基质修饰和炎症的影响。解整合素金属蛋白酶(ADAMs)可能会揭示 AA 和升主动脉夹层(AD)之间的差异。我们对 AD 和 AA 的炎症组织学进行了表征,并研究了 ADAM8 和 -15 在这些疾病中的作用。

材料和方法

对连续 40 例因 AA 或 AD 接受手术的患者的主动脉壁组织学和白细胞、T 和 B 淋巴细胞、浆细胞、巨噬细胞、内皮细胞、平滑肌细胞、细胞增殖、弹性蛋白酶和 Van-Gieson 染色的免疫组织化学进行了分析。使用 QRT-PCR 和免疫组织化学评估了 ADAM8 和 -15 的 mRNA 和蛋白表达。

结果

共纳入 34 例患者,其中 29 例为 AA,5 例为升主动脉 AD。与 AA 相比,AD 患者的全主动脉壁 B 细胞和内膜浆细胞数量更多(p < 0.05)。与 AD 相比,AA 中 ADAM8 和 -15 的基因表达明显降低。AA 中 ADAM8 和 -15 的下调中位数分别为 -2.7 和 -1.8。ADAM8 和 -15 主要存在于 AD 患者的中膜层。2 例 AA 患者的 ADAMs 增加,发展为其余主动脉的 AD。

结论

ADAM8 和 -15 的参与以及包括 B 细胞在内的炎症可能表明主动脉壁的活跃重塑导致 AD。

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