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The multitasking role of macrophages in Stanford type A acute aortic dissection
Flavia Del Porto1, Cira di Gioia, Luigi Tritapepe
1Dipartimento di Medicina Clinica e Molecolare, Facoltà di Medicina e Psicologia, Ospedale Sant'Andrea, Rome, Italy.
Objectives:
The aim of the study was to determine whether the release by macrophages of matrix metalloproteinase (MMP)-12 and vascular endothelial growth factor (VEGF) - leading to inflammation, matrix degradation and neoangiogenesis - represents an effective pathway that underlies aortic wall remodeling in Stanford type A acute aortic dissection (AAD).
Methods:
Twenty-one consecutive patients with no genetic predisposition, with Stanford type A AAD were selected. In each patient, the levels of serum VEGF, MMP-12, serum interleukin (IL)-6, IL-8 and monocyte chemoattractant protein (MCP)-1 were evaluated using enzyme-linked immunosorbent assay. Ascending aortic specimens were collected for immunohistochemical identification of any presence of inflammatory infiltrate, VEGF and CD31 expression.
Results:
A significant increase in serum VEGF (p = 0.044), MMP-12 (p = 0.007), IL-6 (p = 0.0001), IL-8 (p = 0.0001) and MCP-1 (p = 0.0001) levels was observed in the AAD group compared to the control group. Furthermore, all AAD samples were positive for VEGF in the tunica media and showed vessel growth and immune-inflammatory infiltrate. A large number of cases (62.79%) showed inflammation at the edge of the dissection and approximately half (51.42%) showed neovessels growing at the edge of the dissection.
Conclusions:
The results suggest that VEGF-mediated angiogenesis and matrix degradation play a role in AAD. Finally, we believe that MMP-12 should be considered a marker of AAD.
Insights
Vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP)-12 are elevated in acute aortic dissection (AAD), indicating their role in aortic wall remodeling and inflammation. MMP-12 may serve as a diagnostic marker for AAD.
Area of Science:
- Cardiovascular Biology
- Vascular Inflammation
- Aortic Disease
Background:
- Stanford type A acute aortic dissection (AAD) involves complex aortic wall remodeling.
- Macrophages release matrix metalloproteinase (MMP)-12 and vascular endothelial growth factor (VEGF), contributing to inflammation and tissue degradation.
Purpose of the Study:
- To investigate the role of MMP-12 and VEGF in the pathogenesis of AAD.
- To determine if macrophage-derived MMP-12 and VEGF are key mediators of aortic wall remodeling in AAD.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to measure serum levels of VEGF, MMP-12, IL-6, IL-8, and MCP-1 in 21 AAD patients and controls.
- Immunohistochemistry was performed on ascending aortic specimens to assess VEGF, CD31 expression, and inflammatory infiltrate.
Main Results:
- AAD patients exhibited significantly elevated serum levels of VEGF, MMP-12, IL-6, IL-8, and MCP-1 compared to controls.
- AAD aortic tissues showed VEGF expression, neovascularization (CD31+), and immune-inflammatory infiltrates.
- Inflammation and neovessels were observed at the dissection edge in a significant proportion of AAD cases.
Conclusions:
- VEGF-mediated angiogenesis and matrix degradation are implicated in the pathophysiology of AAD.
- MMP-12 is suggested as a potential biomarker for diagnosing AAD.
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