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
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.