摘要
背景:对于急性肺损伤(ALI)并发急性主动脉夹层(AAD)的发病机制知之甚少。 目的:探讨巨噬细胞源性基质金属蛋白酶9(MMP 9)在ALI并发AAD发病中的作用及其参与巨噬细胞增殖的因素。sinister (Latin=left) (拉丁语)左边(的),左派(的) 方法:本研究包括三部分:(1)AAD合并ALI或AAD的非破裂型慢性主动脉瘤患者血清MMPs、血管紧张素Ⅱ(Angii)和MCP-1的测定。(2)用血管紧张素Ⅱ(Angii)注入β-氨基丙腈单抗治疗未成熟大鼠,建立一种新的AAD并发ALI模型。目的探讨MMP 9和MCP-1在AAD并发ALI中的潜在作用。(3)体外培养的肺微血管内皮细胞(PMVEC)系研究了血管内皮细胞(Angii W)的变化。参与大鼠肺血管内皮细胞MCP-1的释放。 结果:AAD合并ALI患者血清MMP 9、Angii、MCP-1明显升高.。MMP 9在肺组织中的表达来源于巨噬细胞。在动物模型中,巨噬细胞MMP 9的释放最终导致ALI,而MMP 9和MCP-1的抑制则导致AAD并发ALI的发生率降低。体外实验表明:通过激活NF-κB信号通路,使PMVECs中MCP-1的过度表达。 结论:AAD合并ALI与巨噬细胞浸润肺间质组织密切相关,并在血管紧张素Ⅱ的作用下释放MMP 9。mcp-1密切相关。来招募巨噬细胞。
关键词: 急性主动脉夹层,急性肺损伤,巨噬细胞MMP9、angiotensin II、MCP-1。
Current Molecular Medicine
Title:A Novel Finding: Macrophages Involved in Inflammation Participate in Acute Aortic Dissection Complicated with Acute Lung Injury
Volume: 17 Issue: 8
关键词: 急性主动脉夹层,急性肺损伤,巨噬细胞MMP9、angiotensin II、MCP-1。
摘要: Background: Little is known about the pathogenesis of acute lung injury (ALI) complicated with acute aortic dissection (AAD).
Objective: We aim to investigate the roles of macrophages-derived matrix metalloproteinase 9 (MMP9) in the development of ALI complicated with AAD and factors involved in the recruitment of macrophages.
Methods: This study included three parts: (i) Determination of serum MMPs, angiotensin II (AngII) and MCP-1 in patients with AAD complicated with ALI or AAD only, non-ruptured chronic aortic aneurysm patients or healthy volunteers using ELISA method. (ii) A novel AAD complicated with ALI model was established by infusing angiotensin II (AngII) to immature rats treated with β-aminopropionitrile monofumarate (BAPN) to identify the potential roles of MMP9 and MCP-1 in AAD complicated with ALI. (iii) Cultured pulmonary microvascular endothelial cell (PMVEC) line was used to investigate how AngII was involved in the release of MCP-1 in rat pulmonary vascular endothelial cells.
Results: Serum MMP9, AngII and MCP-1 were remarkably elevated in patients with AAD complicated with ALI. The MMP9 expressed in pulmonary tissues was derived from macrophages. In the animal model, the release of MMP9 from macrophages finally resulted in ALI, while inhibition of MMP9 and MCP-1 contributed to decreased incidence of AAD complicated with ALI. In vitro experiments indicated that AngII triggered overexpression of MCP-1 in PMVECs by activating NF-κB signaling pathway.
Conclusion: AAD complicated with ALI is highly associated with the macrophages infiltrating the pulmonary interstitial tissue and released MMP9 in response to angiotensin II. MCP-1 is closely related to the recruitment of macrophages.
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Cite this article as:
A Novel Finding: Macrophages Involved in Inflammation Participate in Acute Aortic Dissection Complicated with Acute Lung Injury, Current Molecular Medicine 2017; 17 (8) . https://dx.doi.org/10.2174/1566524018666180222123518
DOI https://dx.doi.org/10.2174/1566524018666180222123518 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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