Adventitial inflammation: A possible pathogenic link to the instability of atherosclerotic plaque

Hu, Cheng Lin; Xiang, Ji Zhou; Hu, Fei; Huang, Chuanhe

doi:10.1016/j.mehy.2006.10.046

Cited by 12 publications

(2 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…10,[25][26][27][28][29][30][31] Not only the intima, but also the deep vascular layers may play a substantial role in plaque formation. 21,[32][33][34][35] We note that the MCIs were localized diffusely in the fibrofatty tissue and/or around the vasa vasorum. The vasa vasorum may be involved in the inflammatory process and in the pathogenesis of atherosclerosis.…”

Section: Discussionmentioning

confidence: 75%

Inflammatory Cell Infiltrates in Vessels With Different Susceptibility to Atherosclerosis in Rheumatic and Non-Rheumatic Patients A Controlled Study of Biopsy Specimens Obtained at Coronary Artery Surgery

Hollan

Prayson

Saatvedt³

et al. 2008

Circ J

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 75%

Inflammatory Cell Infiltrates in Vessels With Different Susceptibility to Atherosclerosis in Rheumatic and Non-Rheumatic Patients A Controlled Study of Biopsy Specimens Obtained at Coronary Artery Surgery

Hollan

Prayson

Saatvedt³

et al. 2008

Circ J

View full text Add to dashboard Cite

“…Although to a lesser extent compared with thrombosed plaques, most mast cells have been reported in the adventitia of intact plaques around microvessels , which is also the site where we observed most MCETs. Therefore, it is conceivable that their traps stimulate pro‐inflammatory functions in the periadventitial fat .…”

Section: Discussionmentioning

confidence: 99%

Extracellular traps derived from macrophages, mast cells, eosinophils and neutrophils are generated in a time‐dependent manner during atherothrombosis

Pertiwi

Boer

Mackaaij

et al. 2019

The Journal of Pathology

128

102

View full text Add to dashboard Cite

Extracellular traps generated by neutrophils contribute to thrombus progression in coronary atherosclerotic plaques. It is not known whether other inflammatory cell types in coronary atherosclerotic plaque or thrombus also release extracellular traps. We investigated their formation by macrophages, mast cells, and eosinophils in human coronary atherosclerosis, and in relation to the age of thrombus of myocardial infarction patients. Coronary arteries with thrombosed or intact plaques were retrieved from patients who died from myocardial infarction. In addition, thrombectomy specimens from patients with myocardial infarction were classified histologically as fresh, lytic or organised. Neutrophil and macrophage extracellular traps were identified using sequential triple immunostaining of CD68, myeloperoxidase, and citrullinated histone H3. Eosinophil and mast cell extracellular traps were visualised using double immunostaining for eosinophil major basic protein or tryptase, respectively, and citrullinated histone H3. Single‐ and double‐stained immunopositive cells in the plaque, adjacent adventitia, and thrombus were counted. All types of leucocyte‐derived extracellular traps were present in all thrombosed plaques, and in all types of the in vivo‐ derived thrombi, but only to a much lower extent in intact plaques. Neutrophil traps, followed by macrophage traps, were the most prominent types in the autopsy series of atherothrombotic plaques, including the adventitia adjacent to thrombosed plaques. In contrast, macrophage traps were more numerous than neutrophil traps in intact plaques (lipid cores) and organised thrombi. Mast cell and eosinophil extracellular traps were also present, but sparse in all instances. In conclusion, not only neutrophils but also macrophages, eosinophils, and mast cells are sources of etosis involved in evolving coronary thrombosis. Neutrophil traps dominate numerically in early thrombosis and macrophage traps in late (organising) thrombosis, implying that together they span all the stages of thrombus progression and maturation. © 2018 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

show abstract

Extracellular Matrix Remodeling in Takayasu's Arteritis: Role of Matrix Metalloproteinases and Adventitial Inflammation

Mahajan¹,

Dhawan²,

Mahmood³

et al. 2012

Archives of Medical Research

View full text Add to dashboard Cite

Adventitial inflammation: A possible pathogenic link to the instability of atherosclerotic plaque

Cited by 12 publications

References 15 publications

Inflammatory Cell Infiltrates in Vessels With Different Susceptibility to Atherosclerosis in Rheumatic and Non-Rheumatic Patients A Controlled Study of Biopsy Specimens Obtained at Coronary Artery Surgery

Inflammatory Cell Infiltrates in Vessels With Different Susceptibility to Atherosclerosis in Rheumatic and Non-Rheumatic Patients A Controlled Study of Biopsy Specimens Obtained at Coronary Artery Surgery

Extracellular traps derived from macrophages, mast cells, eosinophils and neutrophils are generated in a time‐dependent manner during atherothrombosis

Extracellular Matrix Remodeling in Takayasu's Arteritis: Role of Matrix Metalloproteinases and Adventitial Inflammation

Contact Info

Product

Resources

About