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9. Impact of Notch3 Activation on Aortic Aneurysm Development in Marfan Syndrome

Author

Jespersen, Kathryn, primary, Li, Chenxin, additional, Batra, Rishi, additional, Stephenson, Christopher A., additional, Harding, Paul, additional, Sestak, Kylie, additional, Foley, Ryan T., additional, Greene, Harrison, additional, Meisinger, Trevor, additional, Cook, Jason R., additional, Baxter, B. Timothy, additional, and Xiong, Wanfen, additional

Published
2022
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11. Mast cells modulate the pathogenesis of elastase-induced abdominal aortic aneurysms in mice

Author

Sun, Jiusong, Sukhova, Galina K., Yang, Min, Wolters, Paul J., MacFarlane, Lindsey A., Libby, Peter, Sun, Chongxiu, Zhang, Yadong, Liu, Jian, Ennis, Terri L., Knispel, Rebecca, Xiong, Wanfen, Thompson, Robert W., Baxter, B. Timothy, and Shi, Guo-Ping

Subjects
Abdominal aneurysm -- Research, Abdominal aneurysm -- Physiological aspects, Mast cells -- Research, Mast cells -- Observations, Cell research
Abstract

Abdominal aortic aneurysm (AAA), an inflammatory disease, involves leukocyte recruitment, immune responses, inflammatory cytokine production, vascular remodeling, neovascularization, and vascular cell apoptosis, all of which contribute to aortic dilatation. This [...]

Published
2007

29. Correction: Premature aortic smooth muscle cell differentiation contributes to matrix dysregulation in Marfan Syndrome

Author

Dale, Matthew, primary, Fitzgerald, Matthew P., additional, Liu, Zhibo, additional, Meisinger, Trevor, additional, Karpisek, Andrew, additional, Purcell, Laura N., additional, Carson, Jeffrey S., additional, Harding, Paul, additional, Lang, Haili, additional, Koutakis, Panagiotis, additional, Suh, Melissa, additional, Batra, Rishi, additional, Mietus, Constance J., additional, Casale, George, additional, Pipinos, Iraklis, additional, Baxter, B. Timothy, additional, and Xiong, Wanfen, additional

Published
2018
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32. Premature aortic smooth muscle cell differentiation contributes to matrix dysregulation in Marfan Syndrome

Author

Dale, Matthew, primary, Fitzgerald, Matthew P., additional, Liu, Zhibo, additional, Meisinger, Trevor, additional, Karpisek, Andrew, additional, Purcell, Laura N., additional, Carson, Jeffrey S., additional, Harding, Paul, additional, Lang, Haili, additional, Koutakis, Panagiotis, additional, Batra, Rishi, additional, Mietus, Constance J., additional, Casale, George, additional, Pipinos, Iraklis, additional, Baxter, B. Timothy, additional, and Xiong, Wanfen, additional

Published
2017
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33. CD95-ligand contributes to abdominal aortic aneurysm progression by modulating inflammation.

Author

Liu, Zhibo, Fitzgerald, Matthew, Meisinger, Trevor, Batra, Rishi, Suh, Melissa, Greene, Harrison, Penrice, Alexander J, Sun, Lijun, Baxter, B Timothy, and Xiong, Wanfen

Subjects
AORTIC aneurysms, WESTERN immunoblotting, MUSCLE cells, INFLAMMATORY mediators, PROTEOLYSIS, EXTRACELLULAR matrix proteins
Abstract

Aims Abdominal aortic aneurysm (AAA) is one of the number of diseases associated with a prominent inflammatory cell infiltration, matrix protein degradation, and smooth muscle cell apoptosis. CD95 is an inflammatory mediator and an apoptosis inducer. Previous studies have shown elevated expression of CD95 or CD95L in the aortic tissue of AAA patients. However, how the CD95L/CD95 contributes to aneurysm degeneration and whether blocking its signalling would be beneficial to disease progression remains largely unknown. In the present study, we sought to determine the role of CD95L and its downstream target, caspase 8, in AAA progression. Methods and results By using the CaCl2 murine model of AAA, abdominal aortic aneurysms were induced in C57BL/6 mice. We found that both mRNA and protein levels of CD95L were increased in aneurysm tissue compared with NaCl-treated normal aortic tissue. To determine whether CD95L contributes directly to aneurysm formation, we used CD95L null (CD95L−/−) mice to examine their response to CaCl2 aneurysm induction. Six weeks after periaortic application of CaCl2, aortic diameters of CD95L−/− mice were significantly smaller compared to CaCl2-treated wild-type controls. Connective tissue staining of aortic sections from CaCl2-treated CD95L−/− mice showed minimal damage of medial elastic lamellae which was indistinguishable from the NaCl-treated sham control. Furthermore, CD95L deficiency attenuates macrophage and T cell infiltration into the aortic tissue. To study the role of CD95L in the myelogeous cells in AAA formation, we created chimaeric mice by infusing CD95L−/− bone marrow into sub-leathally irradiated wild-type mice (WT/CD95L−/−BM). As controls, wild-type bone marrow were infused into sub-leathally irradiated CD95L−/− mice (CD95L−/−/WTBM). WT/CD95L−/−BM mice were resistant to aneurysm formation compared to their controls. Inflammatory cell infiltration was blocked by the deletion of CD95L on myeloid cells. Western blot analysis showed the levels of caspase 8 in the aortas of CaCl2-treated wild-type mice were increased compared to NaCl-treated controls. CD95L deletion inhibited caspase 8 expression. Furthermore, a caspase 8-specific inhibitor was able to partially block aneurysm development in CaCl2-treated aneurysm models. Conclusion These studies demonstrated that inflammatory cell infiltration during AAA formation is dependent on CD95L from myelogeous cells. Aneurysm inhibition by deletion of CD95L is mediated in part by down-regulation of caspase 8. [ABSTRACT FROM AUTHOR]

Published
2019
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41. Blocking TNF-α Attenuates Aneurysm Formation in a Murine Model1

Author

Xiong, Wanfen, MacTaggart, Jason, Knispel, Rebecca, Worth, Jennifer, Persidsky, Yuri, and Baxter, B. Timothy

Subjects
Mice, Knockout, Tumor Necrosis Factor-alpha, Macrophages, Matrix Metalloproteinase Inhibitors, Elastic Tissue, Article, Muscle, Smooth, Vascular, Mice, Inbred C57BL, Disease Models, Animal, Mice, Cell Migration Inhibition, cardiovascular system, Animals, Humans, Matrix Metalloproteinase 2, cardiovascular diseases, Inflammation Mediators, Cells, Cultured, Aortic Aneurysm, Abdominal, Cell Line, Transformed
Abstract

Abdominal aortic aneurysm (AAA) is one of a number of diseases associated with a prominent inflammatory cell infiltrate and local destruction of structural matrix macromolecules. This chronic infiltrate is predominately composed of macrophages and T lymphocytes. Activated macrophages produce a variety of cytokines, including TNF-alpha. Elevated levels of TNF-alpha were observed in patients with AAA, suggesting that TNF-alpha may play a role in the pathogenic mechanisms of AAA. In the present study, we investigated the role of TNF-alpha in AAA formation. By studying a murine aneurysm model, we found that both mRNA and protein levels of TNF-alpha were increased in aneurysm tissue compared with normal aortic tissues. Therefore, we tested the response of mice lacking expression of TNF-alpha. These mice were resistant to aneurysm formation. Our results show that TNF-alpha deficiency attenuates matrix metalloproteinase (MMP) 2 and MMP-9 expression and macrophage infiltration into the aortic tissue. These data suggest that TNF-alpha plays a central role in regulating matrix remodeling and inflammation in the aortic wall leading to AAA. In addition, we investigated the pharmacological inhibition of AAA. A Food and Drug Administration-approved TNF-alpha antagonist, infliximab, inhibited aneurysm growth. Our data also show that infliximab treatment attenuated elastic fiber disruption, macrophage infiltration, and MMP-2 and MMP-9 expression in aortic tissue. This study confirms that a strategy of TNF-alpha antagonism may be an important therapeutic strategy for treating AAA.

Published
2009

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