Monocyte activity is linked with abdominal aortic aneurysm diameter

Samadzadeh, Kiana M.; Chun, Kevin C.; Nguyen, Anthony T.; Baker, Pamela M.; Bains, Sukhmine; Lee, Eugene S.

doi:10.1016/j.jss.2014.03.019

Cited by 28 publications

(18 citation statements)

References 26 publications

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“…Circulating monocytes from AAA patients displayed enhanced adhesive activity to the endothelial cell wall and increased MMP-9 production. 84 Although these monocytes were not studied specifically for M1 or M2 markers, their presence suggests a systemic inflammatory response, which would be expected due to the presence of high levels of MMP-9 resulting in tissue breakdown. Hance et al demonstrated that monocyte chemotaxis to AAA tissue can be directly linked to breakdown of the ECM, specifically via a six-peptide sequence (VGVAPG) found mainly in elastin.…”

Section: Macrophage Phenotypes: M1 and M2mentioning

confidence: 99%

Inflammatory Cell Phenotypes in AAAs

Dale

Ruhlman

Baxter

2015

ATVB

184

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Abdominal aortic aneurysms are characterized by chronic inflammatory cell infiltration. AAA is typically an asymptomatic disease and caused approximately 15,000 deaths annually in the U.S. Previous studies have examined both human and murine aortic tissue for the presence of various inflammatory cell types. Studies show that in both human and experimental AAAs, prominent inflammatory cell infiltration, such as CD4+ T cells and macrophages, occurs in the damaged aortic wall. These cells have the ability to undergo phenotypic modulation based on microenvironmental cues, potentially influencing disease progression. Pro-inflammatory CD4+ T cells and classically activated macrophages dominate the landscape of aortic infiltrates. The skew to pro-inflammatory phenotypes alters disease progression and plays a role in causing chronic inflammation. The local cytokine production and presence of inflammatory mediators, such as extracellular matrix breakdown products, influence the uneven balance of the inflammatory infiltrate phenotypes. Understanding and developing new strategies that target the pro-inflammatory phenotype could provide useful therapeutic targets for a disease with no current pharmacological intervention.

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Section: Macrophage Phenotypes: M1 and M2mentioning

confidence: 99%

Inflammatory Cell Phenotypes in AAAs

Dale

Ruhlman

Baxter

2015

ATVB

184

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“…First, factors shown to be involved in the development of AAA might eventually serve as biomarkers to identify patients at risk for later AAA formation and to predict the course of disease. Regarding myeloid cells, changes in circulating monocyte subsets (40) or variations in gene or protein expression (115) potentially might serve as predictors for AAA growth. Diminished catalase levels in circulating polymorphonuclear neutrophils and plasma were found to be associated with the presence of AAA (107).…”

Section: Discussionmentioning

confidence: 99%

Involvement of Myeloid Cells and Noncoding RNA in Abdominal Aortic Aneurysm Disease

Knappich

Spin

Eckstein

et al. 2020

Antioxidants & Redox Signaling

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Significance: Abdominal aortic aneurysm (AAA) is a potentially fatal condition, featuring the possibility of high-mortality rupture. To date, prophylactic surgery by means of open surgical repair or endovascular aortic repair at specific thresholds is considered standard therapy. Both surgical options hold different risk profiles of short-and long-term morbidity and mortality. Targeting early stages of AAA development to decelerate disease progression is desirable. Recent Advances: Understanding the pathomechanisms that initiate formation, maintain growth, and promote rupture of AAA is crucial to developing new medical therapeutic options. Inflammatory cells, in particular macrophages, have been investigated for their contribution to AAA disease for decades, whereas evidence on lymphocytes, mast cells, and neutrophils is sparse. Recently, there has been increasing interest in noncoding RNAs (ncRNAs) and their involvement in disease development, including AAA. Critical Issues: The current evidence on myeloid cells and ncRNAs in AAA largely originates from small animal models, making clinical extrapolation difficult. Although it is feasible to collect surgical human AAA samples, these tissues reflect end-stage disease, preventing examination of critical mechanisms behind early AAA formation. Future Directions: Gaining more insight into how myeloid cells and ncRNAs contribute to AAA disease, particularly in early stages, might suggest nonsurgical AAA treatment options. The utilization of large animal models might be helpful in this context to help bridge translational results to humans. Antioxid. Redox Signal. 00, 000-000.

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“…Investigation of human aneurysm tissue has revealed an M1 phenotype, though this tissue represents an end stage of the disease. Most human studies have focused on circulating monocytes and their link to increased elastases and ECM breakdown [30]. ECM breakdown is a recruiter of monocytes, and the use of a monoclonal antibody has been shown to decrease this iniltration and prevent further ECM degradation [31].…”

Section: Macrophagesmentioning

confidence: 99%

Inflammatory Mediators in Abdominal Aortic Aneurysms

Cassimjee¹,

Lee²,

Patel³

2017

Aortic Aneurysm

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Aortic wall dilatation in abdominal aortic aneurysms is characterized by extracellular matrix degradation together with a loss of smooth muscle cells from the aortic media. This occurs in conjunction with a marked inlammatory cell iniltration. The inlammatory cell is characteristic of the second phase of aneurysmal development-progression. It is widely accepted that usually there are three phases involved in the development of abdominal aortic aneurysms: initiation, progression and rupture. In this chapter, we present an overview of the inlammatory mediators in abdominal aortic aneurysms and intraluminal thrombus, highlighting evidence from experimental models and human disease.

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Monocyte activity is linked with abdominal aortic aneurysm diameter

Cited by 28 publications

References 26 publications

Inflammatory Cell Phenotypes in AAAs

Inflammatory Cell Phenotypes in AAAs

Involvement of Myeloid Cells and Noncoding RNA in Abdominal Aortic Aneurysm Disease

Inflammatory Mediators in Abdominal Aortic Aneurysms

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