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TSG-6 is highly expressed in human abdominal aortic aneurysms
S Keisin Wang1, Jie Xie1, Linden A Green1
1Indiana University School of Medicine, Richard Roudebush Veteran Affairs Medical Center, Department of Surgery, Division of Vascular Surgery and Center for Aortic Disease, Indianapolis, Indiana.
The Journal of Surgical Research
|November 29, 2017
Summary
Tumor necrosis factor-stimulated gene-6 (TSG-6) is elevated in abdominal aortic aneurysms (AAA), contributing to inflammation and vessel breakdown. This study investigates TSG-6
Area of Science:
- Vascular Biology
- Immunology
- Atherosclerosis Research
Background:
- Abdominal aortic aneurysms (AAA) involve proinflammatory processes leading to smooth muscle cell apoptosis and matrix degradation.
- Defects in anti-inflammatory responses are implicated in AAA but require further characterization.
- Tumor necrosis factor-stimulated gene-6 (TSG-6) is an anti-inflammatory protein involved in matrix stabilization and cell migration.
Purpose of the Study:
- To investigate the role of TSG-6 in the pathogenesis of abdominal aortic aneurysms (AAA).
- To quantify TSG-6 levels in AAA patients and healthy controls.
- To determine the cellular localization and functional impact of TSG-6 in AAA.
Main Methods:
- Collection of blood and aortic tissue samples from organ donors, AAA screening subjects, and AAA repair patients.
- Assay of protein concentrations in tissue and plasma using ELISA.
- Flow cytometry (FACS) for immune cell populations and in vitro macrophage polarization assays.
Main Results:
- TSG-6 was significantly elevated in plasma and aortic walls of AAA patients compared to controls.
- Highest TSG-6 concentrations were found in aneurysm shoulders, localized to the tunica media.
- TSG-6 inhibited the in vitro polarization of anti-inflammatory M2 macrophages.
Conclusions:
- AAA formation is linked to an inflammatory imbalance and mononuclear cell infiltration.
- Elevated TSG-6 expression in the aortic wall and circulation is a hallmark of the AAA condition.
- TSG-6 may play a critical role in modulating the inflammatory response within AAA.
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