Inflammation in abdominal aortic aneurysms: cellular infiltrate and cytokine profiles

Vascular ◽  
2012 ◽  
Vol 20 (5) ◽  
pp. 278-283 ◽  
Author(s):  
Matthew J Eagleton
Keyword(s):  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Wall Stress ◽  
Aortic Aneurysms ◽  
Aneurysm Formation ◽  
Abdominal Aortic ◽  
Genetic Abnormalities ◽  
Cytokine Milieu ◽  
Ultimate Fate ◽  
Pathologic Processes

Abdominal aortic aneurysm (AAA) pathogenesis occurs as a result of the altered homeostasis of the aortic vessel wall structural proteins. This results in weakening, and subsequent expansion, of the aorta leading to aneurysm formation. Multiple mechanisms are involved in this process, including genetic abnormalities, biomechanical wall stress, apoptosis, and proteolytic degradation of the aortic wall. One key hallmark of this pathology, which orchestrates the interaction of the various pathologic processes, is inflammation. The inflammatory process is characterized by the infiltration of a variety of cells, which leads to the upregulation of multiple cytokines. The balance of the cellular type and resultant cytokine milieu determines the ultimate fate of the aortic wall – healing, atherosclerosis or aneurysm formation. This review highlights some of the known cellular and cytokine inflammatory events that are involved in aortic aneurysm formation.

Abstract 297: Segmental Aortic Stiffening is a Mechanism Driving Early Abdominal Aortic Aneurysm Pathogenesis

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Uwe Raaz ◽  
Alexander M Zöllner ◽  
Ryuji Toh ◽  
Futoshi Nakagami ◽  
Isabel N Schellinger ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Ex Vivo ◽  
Wall Stress ◽  
Finite Elements Analysis ◽  
External Application ◽  
Abdominal Aortic ◽  
Aneurysm Growth ◽  
Aortic Stiffening

Stiffening of the aortic wall is a phenomenon consistently observed in abdominal aortic aneurysm (AAA). However, its role in AAA pathophysiology is largely undefined. Using an established murine elastase-induced AAA model, we demonstrate that segmental aortic stiffening (SAS) precedes aneurysm growth. Finite elements analysis (FEA)-based wall stress calculations reveal that early stiffening of the aneurysm-prone aortic segment leads to axial (longitudinal) stress generated by cyclic (systolic) tethering of adjacent, more compliant wall segments. Interventional stiffening of AAA-adjacent segments (via external application of surgical adhesive) significantly reduces aneurysm growth. These changes correlate with reduced segmental stiffness of the AAA-prone aorta (due to equalized stiffness in adjacent aortic segments), reduced axial wall stress, decreased production of reactive oxygen species (ROS), attenuated elastin breakdown, and decreased expression of inflammatory cytokines and macrophage infiltration, as well as attenuated apoptosis within the aortic wall. Cyclic pressurization of stiffened aortic segments ex vivo increases the expression of genes related to inflammation and extracellular matrix (ECM) remodeling. Finally, human ultrasound studies reveal that aging, a significant AAA risk factor, is accompanied by segmental infrarenal aortic stiffening. The present study introduces the novel concept of segmental aortic stiffening (SAS) as an early pathomechanism generating aortic wall stress and thereby triggering AAA growth. Therefore monitoring SAS by ultrasound might help to better identify patients at risk for AAA disease and better predict the susceptibility of small AAA to further growth. Moreover our results suggest that interventional mechanical stiffening of the AAA-adjacent aorta may be further tested as a novel treatment option to limit early AAA growth.

Abstract 667: The Role of Aortic Wall-Nuclear Factor- kappa B (NF-kB) Signaling in Formation of Dissecting Aortic Aneurysms

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Talha Ijaz ◽  
Hong Sun ◽  
Adrian Recinos ◽  
Ronald G Tilton ◽  
Allan R Brasier
Keyword(s):  
Flow Cytometry ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Aortic Rupture ◽  
Aortic Aneurysms ◽  
Tunel Staining ◽  
Abdominal Aortic ◽  
Significant Difference

Introduction: Abdominal aortic aneurysm is a devastating disease since it can lead to aortic rupture and instantaneous death. We previously demonstrated that IL-6 secreted from the aortic wall is necessary for the development of abdominal aortic aneurysm and dissection (AAD). Since IL-6 is a NF-kB/RelA dependant gene, we investigated the role of aortic wall- NF-kB/RelA signaling in the development of AAD. Methods and Results: To test the role of aortic wall-RelA, we utilized Cre-Lox technology to delete RelA from aortic cells. Tamoxifen-inducible, Col1a2-promoter driven Cre mice (Col1a2-Cre) were crossed with mT/mG Cre-reporter mice to determine which aortic cells undergo genetic recombination after Cre activation. Flow cytometry analysis of the aortic wall indicated that 88% of the genetically recombined cells were SMCs and 8% were fibroblasts. Next, RelA floxed (RelA f/f) mice, generated in our lab, were crossed with Col1a2-Cre mice. RelA f/f Cre+ and RelA f/f Cre- were stimulated with tamoxifen for 10 days to generate aortic-RelA deficient (Ao-RelA-/-) or wild-type (Ao-RelA+/+) transgenics. Flow cytometry, qRT-PCR, and immunohistochemistry analysis suggested a depletion of aortic-RelA greater than 60%. To test the role of Ao-RelA in AAD, Ao-RelA -/- (n= 20) and Ao-RelA +/+ (n=14) mice were infused with angiotensin II for 7 days. Surprisingly, 20% of Ao-RelA-/- mice died from development of AAD and aortic rupture while no deaths were observed in Ao-RelA+/+ group. In addition, 40% of Ao-RelA-/- mice developed AAD compared to 14% of Ao-RelA+/+ mice. There was no significant difference in TUNEL staining or ERTR7+ fibroblast population between the two groups. Conclusion: Our studies suggest that aortic wall-RelA may be necessary for protection from AAD.

A COMPUTATIONAL MODEL OF BLOOD FLOW AND AORTIC WALL STRESS IN ABDOMINAL AORTIC ANEURYSMS

ASAIO Journal ◽  
1999 ◽  
Vol 45 (2) ◽  
pp. 197
Author(s):  
P J Cabrales ◽  
J E Gómez ◽  
J Camacho ◽  
C Espinel ◽  
J C Briceño
Keyword(s):  
Blood Flow ◽  
Computational Model ◽  
Aortic Wall ◽  
Wall Stress ◽  
Abdominal Aortic Aneurysms ◽  
Aortic Aneurysms ◽  
Abdominal Aortic

scholarly journals Analysis of aortic wall stress and rupture risk in patients with abdominal aortic aneurysm with a gender perspective

2011 ◽  
Vol 54 (2) ◽  
pp. 295-299 ◽  
Author(s):  
Emma Larsson ◽  
Fausto Labruto ◽  
T. Christian Gasser ◽  
Jesper Swedenborg ◽  
Rebecka Hultgren
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Wall Stress ◽  
Rupture Risk ◽  
Gender Perspective ◽  
Abdominal Aortic

scholarly journals Estimation of Selected Minerals in Aortic Aneurysms—Impaired Ratio of Zinc to Lead May Predispose?

2020 ◽  
Author(s):  
Katarzyna Socha ◽  
Alicja Karwowska ◽  
Adam Kurianiuk ◽  
Renata Markiewicz-Żukowska ◽  
Andrzej Guzowski ◽  
...  
Keyword(s):  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Average Concentration ◽  
Aortic Aneurysms ◽  
Molar Ratio ◽  
Control Group ◽  
Tissue Samples ◽  
Abdominal Aortic ◽  
Mineral Components ◽  
Cadmium And Lead

Abstract The objective of this study was to estimate the content of copper, zinc, selenium, cadmium, and lead in the tissue of patients with aortic aneurysms. Molar ratio of Cu/Zn and antioxidant micronutrients to toxic elements was also calculated. A total of 108 patients: 47 with abdominal aortic aneurysm (AAA), 61 patients with thoracic aortic aneurysm (TAA), and a control group of 20 abdominal aortic (AA) and 20 thoracic aortic (TA) wall samples from the deceased were studied. The concentrations of mineral components in the tissue samples were determined by the AAS method. The average concentration of Cu in the aortic wall of patients with TAA was significantly lower than in the aortic wall samples of healthy people. The mean concentration of Zn in the aortic wall of patients with AAA and TAA was significantly lower than in the control group samples. Cu/Zn ratio was significantly higher in AAA patients than in control group which indicates a greater role of oxidative stress and inflammatory process in this type of aneurysm. The concentration of Se was significantly decreased in TAA patients compared with the control group; in turn, the concentration of Pb was increased in this group of patients. We observed significantly lower Cu/Pb ratio in TAA patients than in control group, whereas Zn/Pb ratio was significantly lower comparing with control samples in both types of aneurysms. In the examined aneurysms, we have shown the differences in concentrations of mineral components compared with the control tissues. The Zn concentration was decreased in both AAA and TAA samples. Impaired ratio of Zn to Pb may predispose to aortic aneurysms.

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