Related Experiment Video
Updated: Feb 14, 2026
Open Tracheostomy Gastric Acid Aspiration Murine Model of Acute Lung Injury Results in Maximal Acute Nonlethal Lung Injury
Published on: February 26, 2017
A Novel Finding: Macrophages Involved in Inflammation Participate in Acute Aortic Dissection Complicated with Acute
1Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.
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.
Insights
Acute aortic dissection with acute lung injury involves macrophages releasing matrix metalloproteinase 9 (MMP9). Angiotensin II (AngII) drives this process, with MCP-1 recruiting macrophages to the lungs.
Area of Science:
- Cardiovascular Research
- Pulmonary Medicine
- Inflammation Biology
Background:
- Pathogenesis of acute lung injury (ALI) complicating acute aortic dissection (AAD) remains poorly understood.
- Investigating the specific molecular mechanisms linking these two critical conditions is essential for improving patient outcomes.
Purpose of the Study:
- To elucidate the role of macrophage-derived matrix metalloproteinase 9 (MMP9) in the development of ALI in AAD patients.
- To identify factors, particularly angiotensin II (AngII) and MCP-1, involved in macrophage recruitment and activation.
Main Methods:
- Serum levels of MMPs, AngII, and MCP-1 were measured in AAD patients with or without ALI, chronic aneurysm patients, and healthy controls.
- A rat model of AAD with ALI was established to study the roles of MMP9 and MCP-1.
- In vitro studies using pulmonary microvascular endothelial cells (PMVECs) investigated AngII's effect on MCP-1 release via the NF-κB pathway.
Main Results:
- Patients with AAD and ALI exhibited significantly elevated serum MMP9, AngII, and MCP-1 levels.
- MMP9 in lung tissue was confirmed to originate from infiltrating macrophages.
- Inhibition of MMP9 and MCP-1 reduced the incidence of AAD complicated with ALI in the animal model.
- AngII stimulated MCP-1 overexpression in PMVECs by activating the NF-κB signaling pathway.
Conclusions:
- AAD complicated with ALI is strongly associated with macrophage infiltration into lung tissue and MMP9 release, mediated by AngII.
- MCP-1 plays a crucial role in recruiting macrophages to the site of injury, contributing to the pathogenesis of ALI in AAD.
Related Concept Videos
01:22Acute Kidney Injury I: Introduction
01:29Acute Kidney Injury II: Pathophysiology
01:22Acute Kidney Injury VI: Nursing Management
01:38Inflammation
01:20Acute Kidney Injury V: Interprofessional Care
01:29Acute Kidney Injury III: Clinical Manifestations