Neutrophil Extracellular Traps Participate in All Different Types of Thrombotic and Haemorrhagic Complications of Coronary Atherosclerosis

2018 ◽  
Vol 118 (06) ◽  
pp. 1078-1087 ◽  
Author(s):  
Kartika Pertiwi ◽  
Allard van der Wal ◽  
Dara Pabittei ◽  
Claire Mackaaij ◽  
Marinus van Leeuwen ◽  
...  
Keyword(s):  
Acute Coronary Syndromes ◽  
Coronary Atherosclerosis ◽  
Coronary Plaque ◽  
Neutrophil Extracellular Traps ◽  
Arginine Deiminase ◽  
Extracellular Traps ◽  
Fibrous Cap ◽  
Histone 3 ◽  
Different Types ◽  
Coronary Syndromes

AbstractAcute coronary syndromes can be initiated by either atherosclerotic fibrous cap ruptures, superficial plaque erosions or intraplaque haemorrhages (IPHs). Since neutrophil extracellular traps (NETs) display pro-inflammatory and pro-thrombotic properties, we investigated the presence, extent and distribution of neutrophils and NETs in different types of plaque complications in relation to the age of overlying thrombus mass or haemorrhage. Sixty-four paraffin-embedded coronary plaque segments of 30 acute myocardial infarction patients were retrieved from the autopsy archives, which contained 44 complicated plaques (17 IPHs, 9 erosions and 18 ruptures) and 20 intact plaques. Complicated plaques were further categorized according to the histological age of thrombus or haemorrhage. Immunohistochemistry was performed to visualize neutrophils (anti-myeloperoxidase, anti-elastase and anti-CD177) and NETs (anti-citrullinated histone-3 and anti-peptidyl-arginine-deiminase-4). The results were scored semi-quantitatively. Neutrophils and NETs were abundantly present in all types of complicated, but not in intact, plaques (p < 0.05). They were found in thrombus, haemorrhages and at the thrombus–plaque interface, with no significant differences in extent between ruptures, erosions and IPHs. Interestingly, adjacent perivascular tissue of complicated, but not of intact plaques, also contained high numbers of neutrophils and NETs (p < 0.05). In thrombus and haemorrhage of different age, neutrophils and NETs were more frequently present in non-organized (fresh) thrombi and in on-going IPHs. In conclusion, netosis is a prominent pro-thrombotic participant in all distinct types of atherothrombosis, which may facilitate the progression of thrombotic or haemorrhagic complications and thus the onset of ensuing clinical coronary ischemic syndromes.

Temperature Measurement of Advanced Murine Atherosclerotic Plaques

2007 ◽  
Author(s):  
Frank Gijsen ◽  
Anna Ten Have ◽  
Jolanda Wentzel ◽  
Antonius Van Der Steen
Keyword(s):  
Heart Disease ◽  
Vulnerable Plaque ◽  
Acute Coronary Syndromes ◽  
Coronary Atherosclerosis ◽  
Developmental Stages ◽  
Atherosclerotic Plaques ◽  
Fibrous Cap ◽  
Vulnerable Plaques ◽  
Coronary Syndromes ◽  
Plaque Detection

Ischaemic heart disease is most frequently caused by coronary atherosclerosis, of which the vulnerable plaque is one of the developmental stages. Rupture of a vulnerable plaque with superimposed thrombosis frequently leads to acute coronary syndromes. The major components of a vulnerable plaque are a lipid-rich, atheromatous core, and a thin fibrous cap with macrophage and macrophage infiltration (Schaar et al., 2004). After the first paper suggesting the possibility of thermographic detection of vulnerable plaques (Casscells et al., 1996), intracoronary thermography as a vulnerable plaque detection technique has been investigated. Increased metabolic activity of macrophages is suggested as the main reasons for the increased temperatures (ten Have et al., 2005).

scholarly journals Silver Nanoparticles Induce Neutrophil Extracellular Traps Via Activation of PAD and Neutrophil Elastase

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 317
Author(s):  
HanGoo Kang ◽  
Jinwon Seo ◽  
Eun-Jeong Yang ◽  
In-Hong Choi
Keyword(s):  
Silver Nanoparticles ◽  
Neutrophil Elastase ◽  
Mammalian Cells ◽  
Antimicrobial Properties ◽  
Neutrophil Extracellular Traps ◽  
Arginine Deiminase ◽  
Human Neutrophils ◽  
Extracellular Traps ◽  
Peptidyl Arginine Deiminase ◽  
Key Factor

Silver nanoparticles (AgNPs) are widely used in various fields because of their antimicrobial properties. However, many studies have reported that AgNPs can be harmful to both microorganisms and humans. Reactive oxygen species (ROS) are a key factor of cytotoxicity of AgNPs in mammalian cells and an important factor in the immune reaction of neutrophils. The immune reactions of neutrophils include the expulsion of webs of DNA surrounded by histones and granular proteins. These webs of DNA are termed neutrophil extracellular traps (NETs). NETs allow neutrophils to catch and destroy pathogens in extracellular spaces. In this study, we investigated how AgNPs stimulate neutrophils, specifically focusing on NETs. Freshly isolated human neutrophils were treated with 5 or 100 nm AgNPs. The 5 nm AgNPs induced NET formation, but the 100 nm AgNPs did not. Subsequently, we investigated the mechanism of AgNP-induced NETs using known inhibitors related to NET formation. AgNP-induced NETs were dependent on ROS, peptidyl arginine deiminase, and neutrophil elastase. The result in this study indicates that treatment of 5 nm AgNPs induce NET formation through histone citrullination by peptidyl arginine deiminase and histone cleavage by neutrophil elastase.

Impact of glucose-6-phosphate dehydrogenase deficiency on the severity of coronary atherosclerosis in patients with acute coronary syndromes

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Giuseppe D. Sanna ◽  
Mario E. Canonico ◽  
Roberta Siciliano ◽  
Simona Guarino ◽  
Francesco Montereggi ◽  
...  
Keyword(s):  
Acute Coronary Syndromes ◽  
Coronary Atherosclerosis ◽  
Dehydrogenase Deficiency ◽  
Coronary Syndromes ◽  
Glucose 6 Phosphate Dehydrogenase

scholarly journals Gender and the Extent of Coronary Atherosclerosis, Plaque Composition, and Clinical Outcomes in Acute Coronary Syndromes

2012 ◽  
Vol 5 (3) ◽  
pp. S62-S72 ◽  
Author(s):  
Alexandra J. Lansky ◽  
Vivian G. Ng ◽  
Akiko Maehara ◽  
Giora Weisz ◽  
Amir Lerman ◽  
...  
Keyword(s):  
Clinical Outcomes ◽  
Acute Coronary Syndromes ◽  
Coronary Atherosclerosis ◽  
Plaque Composition ◽  
Coronary Syndromes

scholarly journals Correlation of Serum Uric Acid Levels with Nonculprit Plaque Instability in Patients with Acute Coronary Syndromes: A 3-Vessel Optical Coherence Tomography Study

2018 ◽  
Vol 2018 ◽  
pp. 1-7
Author(s):  
Donghui Zhang ◽  
Ruoxi Zhang ◽  
Ning Wang ◽  
Lin Lin ◽  
Bo Yu
Keyword(s):  
Optical Coherence Tomography ◽  
Uric Acid ◽  
Serum Uric Acid ◽  
Elevated Serum ◽  
Coronary Plaque ◽  
Optical Coherence ◽  
Plaque Instability ◽  
Coronary Syndrome ◽  
Fibrous Cap ◽  
Coronary Syndromes

Elevated serum uric acid (SUA) level is known to be a prognostic factor in patients with acute coronary syndrome (ACS). However, the correlation between SUA level and coronary plaque instability has not been fully evaluated. The aim of this study was to investigate the association between SUA level and plaque instability of nonculprit lesions in patients with ACS using optical coherence tomography. A total of 150 patients with ACS who underwent 3-vessel optical coherence tomography were selected. Patients were classified into 3 groups according to tertiles of SUA level. There was a trend towards a thinner fibrous cap (0.15 ± 0.06 versus 0.07 ± 0.01 versus 0.04 ± 0.01 mm2, p<0.001) and a wider mean lipid arc (169.41 ± 33.16 versus 177.22 ± 37.76 versus 222.43 ± 47.65°, p<0.001) with increasing SUA tertile. The plaques of the high and intermediate tertile groups had a smaller minimum lumen area than the low tertile group (6.02 ± 1.11 versus 5.38 ± 1.28 mm2, p<0.001). In addition, thin-cap fibroatheromas, microvessels, macrophages, and cholesterol crystals were more frequent in the high tertile group than the low and intermediate groups. Multivariate analysis showed SUA level to be a predictor of plaque instability.

scholarly journals Neutrophil Extracellular Traps Promote the Development of Intracranial Aneurysm Rupture

Hypertension ◽  
2021 ◽  
Author(s):  
Masaaki Korai ◽  
James Purcell ◽  
Yoshinobu Kamio ◽  
Kazuha Mitsui ◽  
Hajime Furukawa ◽  
...  
Keyword(s):  
Intracranial Aneurysm ◽  
Interleukin 1 ◽  
Neutrophil Extracellular Traps ◽  
Aneurysm Rupture ◽  
Arginine Deiminase ◽  
Intercellular Adhesion Molecule ◽  
Necrosis Factor Alpha ◽  
Extracellular Traps ◽  
Peptidyl Arginine Deiminase ◽  
Aneurysm Wall

Potential roles for neutrophils in the pathophysiology of intracranial aneurysm have long been suggested by clinical observations. The presence of neutrophil enzymes in the aneurysm wall has been associated with significant increases in rupture risk. However, the mechanisms by which neutrophils may promote aneurysm rupture are not well understood. Neutrophil extracellular traps (NETs) were implicated in many diseases that involve inflammation and tissue remodeling, including atherosclerosis, vasculitis, and abdominal aortic aneurysm. Therefore, we hypothesized that NETs may promote the rupture of intracranial aneurysm, and that removal of NETs can reduce the rate of rupture. We employed both pharmacological and genetic approaches for the disruption of NETs and used a mouse model of intracranial aneurysm to investigate the roles of NETs in the development of intracranial aneurysm rupture. Here, we showed that NETs are detected in human intracranial aneurysms. Both global and granulocyte-specific knockout of peptidyl arginine deiminase 4 (an enzyme essential for NET formation) reduced the rate of aneurysm rupture. Pharmacological blockade of the NET formation by Cl-amidine also reduced the rate of aneurysm rupture. In addition, the resolution of already formed NETs by deoxyribonuclease was effective against aneurysm rupture. Inhibition of NETs formation with Cl-amidine decreased mRNA expression of proinflammatory cytokines (intercellular adhesion molecule 1 (ICAM-1), interleukin 1 beta (IL-1β), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor alpha (TNF-α)) in cerebral arteries. These data suggest that NETs promote the rupture of intracranial aneurysm. Pharmacological removal of NETs, by inhibition of peptidyl arginine deiminase 4 or resolution of already-formed NETs, may represent a potential therapeutic strategy for preventing aneurysmal rupture.

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