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ADAMTS-7 的上调和 COMP 的下调与主动脉瘤有关。

Upregulation of ADAMTS‑7 and downregulation of COMP are associated with aortic aneurysm.

机构信息

Department of Cardiothoracic Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.

出版信息

Mol Med Rep. 2017 Oct;16(4):5459-5463. doi: 10.3892/mmr.2017.7293. Epub 2017 Aug 21.

DOI:10.3892/mmr.2017.7293
PMID:28849199
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5647091/
Abstract

Aortic aneurysm (AA) remains a fatal condition with high rates of morbidity and mortality, and the associated underlying mechanism influencing its pathology remains to be elucidated. A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)‑7 has previously been demonstrated to be involved in the pathogenesis of vascular atherosclerosis via degradation of cartilage oligomeric matrix protein (COMP). The ADAMTS‑7/COMP pathway may therefore act as a potential therapeutic target for vascular disorders. To the best of the author's knowledge, the present study aimed to investigate for the first time, the expression of ADAMTS‑7 and COMP in human AA. Human aortic aneurysm samples were collected from patients with AA (n=24), and ascending aorta control samples were harvested from dilated cardiomyopathy patients who underwent heart transplantation (n=18). Expression levels of ADAMTS‑7 and matrix metalloproteinase‑9 were significantly increased in the AA group, as detected by immunohistochemistry (P<0.05). The COMP protein level was markedly decreased in the AA group when compared with the control group, as demonstrated via immunohistochemistry and western blot analysis (P<0.05). The findings suggest that upregulation of ADAMTS‑7 and downregulation of COMP are associated with induction of human AA. ADAMTS‑7/COMP pathway may provide therefore act as a potential therapeutic target in human AA for efficient, optimal treatment interventions in the future.

摘要

腹主动脉瘤(AAA)仍然是一种致命的疾病,其发病率和死亡率都很高,其影响病理学的潜在机制仍有待阐明。解整合素和金属蛋白酶与血小板反应蛋白基序(ADAMTS)-7 先前已被证明通过降解软骨寡聚基质蛋白(COMP)参与血管动脉粥样硬化的发病机制。因此,ADAMTS-7/COMP 途径可能是血管疾病的潜在治疗靶点。据作者所知,本研究首次旨在探讨 ADAMTS-7 和 COMP 在人 AAA 中的表达。从患有 AAA 的患者(n=24)中收集人主动脉瘤样本,并从接受心脏移植的扩张型心肌病患者中采集升主动脉对照样本(n=18)。免疫组织化学检测结果显示,AAA 组 ADAMTS-7 和基质金属蛋白酶-9 的表达水平显著升高(P<0.05)。免疫组织化学和 Western blot 分析显示,AAA 组 COMP 蛋白水平明显低于对照组(P<0.05)。这些发现表明,ADAMTS-7 的上调和 COMP 的下调与人类 AAA 的诱导有关。因此,ADAMTS-7/COMP 途径可能为人类 AAA 提供一个潜在的治疗靶点,以便未来进行有效、最佳的治疗干预。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/5647091/6d4ccc067402/MMR-16-04-5459-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/5647091/18da40f8204e/MMR-16-04-5459-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/5647091/e6413a8d9b5f/MMR-16-04-5459-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/5647091/48708c78655b/MMR-16-04-5459-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/5647091/ee5a4d9a855b/MMR-16-04-5459-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/5647091/cba3f3a70bda/MMR-16-04-5459-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/5647091/6d4ccc067402/MMR-16-04-5459-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/5647091/18da40f8204e/MMR-16-04-5459-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/5647091/e6413a8d9b5f/MMR-16-04-5459-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/5647091/48708c78655b/MMR-16-04-5459-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/5647091/ee5a4d9a855b/MMR-16-04-5459-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/5647091/cba3f3a70bda/MMR-16-04-5459-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/5647091/6d4ccc067402/MMR-16-04-5459-g05.jpg

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