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Updated: Feb 5, 2026

Porcine Model of Infrarenal Abdominal Aortic Aneurysm
Published on: November 21, 2019
Local upregulation of interleukin-1 beta in aortic dissecting aneurysm: correlation with matrix metalloproteinase-2,
Yun-Fei Jiang1, Ling-Ling Guo2, Li-Wei Zhang3
1Department of Vascular Surgery, The First People's Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China.
Objectives:
Our goal was to examine whether interleukin-1 beta (IL-1β) originates locally and its possible relationship with matrix metalloproteinases (MMPs), apoptosis, elastin fibres and biomechanics in aortic dissecting aneurysms (DAs).
Methods:
Aortic DAs were induced in 24 rats with β-aminopropionitrile (BAPN); another 12 rats without BAPN were designated as controls. Then IL-1β levels were measured both in the circulation and in local aortic specimens. The expression of MMP-2 and MMP-9 and Victoria blue and TUNEL staining were also detected. Biomechanical parameters such as the elasticity modulus were used to detect the biomechanical changes in the aortic wall. The correlation of IL-1β, MMP-2, MMP-9, apoptosis and biomechanical properties was analysed.
Results:
Seventeen rats (17/24, 71%) in the BAPN-treated group died of DA rupture. IL-1β levels were dramatically increased in the DA specimens but not in the circulation. Victoria blue staining confirmed the formation of the DA and the reduction of elastin content after induction by BAPN. The extent of apoptosis in the aortic media was dramatically higher in rats with BAPN-induced DA than that in the control group and that in rats treated with BAPN but without DA. MMP-2 and MMP-9 levels were significantly increased in BAPN-treated rats compared to the controls, but no statistical significance was found between rats with and without DA. There were significant differences in biomechanical parameters, such as the elasticity modulus. Among the 3 groups, IL-1β was positively correlated with MMP-2 and MMP-9 levels and with the elasticity modulus but not with apoptosis.
Conclusions:
Local IL-1β might participate in the formation of aortic DA through the upregulation of MMP-2 and MMP-9 and the breakage of elastin fibres, which finally weakens the biomechanical properties of the aortic wall.
Insights
Local interleukin-1 beta (IL-1β) increased in aortic dissecting aneurysms (DAs), correlating with matrix metalloproteinases (MMPs) and weakened biomechanics. This suggests IL-1β contributes to DA formation by degrading elastin and impairing aortic wall strength.
Area of Science:
- Cardiovascular Biology
- Pathology
- Biomedical Engineering
Background:
- Aortic dissecting aneurysms (DAs) are life-threatening conditions characterized by aortic wall weakening.
- The precise molecular mechanisms driving DA pathogenesis, particularly the role of local inflammatory mediators, remain incompletely understood.
Purpose of the Study:
- To investigate the local origin and role of interleukin-1 beta (IL-1β) in the development of aortic dissecting aneurysms (DAs).
- To explore the relationship between IL-1β, matrix metalloproteinases (MMPs), apoptosis, elastin degradation, and biomechanical changes in the aortic wall.
Main Methods:
- Aortic dissecting aneurysms were induced in rats using β-aminopropionitrile (BAPN).
- IL-1β levels were measured in circulation and local aortic tissue.
- Expression of MMP-2 and MMP-9, elastin content, apoptosis, and biomechanical properties (elasticity modulus) were assessed.
Main Results:
- Rats treated with BAPN showed significantly increased IL-1β in aortic tissue but not in circulation.
- Elevated levels of MMP-2 and MMP-9, reduced elastin, and increased apoptosis were observed in BAPN-induced DAs.
- IL-1β positively correlated with MMP-2, MMP-9, and the elasticity modulus, indicating impaired biomechanical properties.
Conclusions:
- Local IL-1β plays a significant role in the pathogenesis of aortic dissecting aneurysms.
- IL-1β may contribute to DA formation by upregulating MMPs, degrading elastin, and compromising aortic wall biomechanics.
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