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Murine Surgical Model of Topical Elastase Induced Descending Thoracic Aortic Aneurysm
Published on: August 24, 2019
Blocking TNF-alpha attenuates aneurysm formation in a murine model
Wanfen Xiong1, Jason MacTaggart, Rebecca Knispel
1Department of Surgery, University of Nebraska Medical Center, Omaha,NE 68198, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|July 22, 2009
Summary
Tumor necrosis factor-alpha (TNF-alpha) drives abdominal aortic aneurysm (AAA) formation by promoting inflammation and matrix degradation. Blocking TNF-alpha with infliximab effectively prevented AAA development in a mouse model.
Area of Science:
- Cardiovascular Biology
- Immunology
- Molecular Medicine
Background:
- Abdominal aortic aneurysm (AAA) involves inflammation and matrix destruction.
- Macrophages and T lymphocytes infiltrate AAA tissue.
- Tumor necrosis factor-alpha (TNF-alpha) is elevated in AAA patients.
Purpose of the Study:
- To investigate the role of TNF-alpha in AAA pathogenesis.
- To evaluate TNF-alpha antagonism as a therapeutic strategy for AAA.
Main Methods:
- Utilized a murine model of AAA.
- Assessed TNF-alpha levels (mRNA and protein) in aneurysm tissue.
- Examined AAA formation in TNF-alpha deficient mice.
- Investigated the effect of infliximab (a TNF-alpha antagonist) on AAA growth and associated molecular changes.
Main Results:
- TNF-alpha levels were significantly increased in AAA tissue.
- Mice lacking TNF-alpha were resistant to AAA formation.
- TNF-alpha deficiency reduced macrophage infiltration and matrix metalloproteinase (MMP) 2 and MMP-9 expression.
- Infliximab treatment inhibited AAA growth, elastic fiber disruption, macrophage infiltration, and MMP expression.
Conclusions:
- TNF-alpha plays a critical role in AAA development by regulating inflammation and matrix remodeling.
- Targeting TNF-alpha with antagonists like infliximab shows therapeutic potential for AAA treatment.
