Coronary Arteries of Cardiac Patients Are Hyperreactive and Contain Stores of Amines: A Mechanism for Coronary Spasm

Kalsner, Stanley; Richards, Robert

doi:10.1126/science.6701530

Cited by 211 publications

(90 citation statements)

References 12 publications

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“…Increased histamine concentration in cardiac tissue also corresponds to increased mast cell density [16]. In clinical situations, the presence of mast cells around and within the coronary blood vessels has been implicated in the pathophysiology of coronary artery disease [31][32][33]. The role of mast cells has been established in myocardial fibrosis in Africans [18], and in dilated cardiomyopathy secondary to systemic sclerosis [34].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of mast cells by interleukin‐10 gene transfer contributes to protection against acute myocarditis in rats

Palaniyandi

Watanabe

et al. 2004

Eur J Immunol

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Progression of acute myocarditis involves a variety of inflammatory events. Mast cells have been implicated as the source of various cytokines, chemokines and histamine in acute inflammation and fibrosis. Interleukin (IL)-10 has well-known immunomodulatory actions that are exerted during the recovery phase of myocarditis. In this study, 9-week-old male Lewis rats were immunized with cardiac myosin. A plasmid vector expressing mouse IL-10 cDNA (800 lg per rat) was then transferred three times (7, 12 and 17 days after immunization) into the tibialis anterior muscles of the rats by electroporation. Microscopic examination of mast cells was carried out on toluidine blue-stained transverse sections of the mid ventricles. Mouse IL-10 gene transfer significantly reduced mast cell density, cardiac histamine concentration and mast cell growth, and prevented mast cell degranulation. Furthermore, improvement in both myocardial function and the overall condition of the rats was evident from the reduction in the heart weight-to-body weight ratio and inflammatory infiltration as well as improvement in hemodynamic and echocardiographic parameters. These findings suggest that IL-10 gene transfer by electroporation protected against myocarditis via mast cell inhibition.

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Section: Discussionmentioning

confidence: 99%

Inhibition of mast cells by interleukin‐10 gene transfer contributes to protection against acute myocarditis in rats

Palaniyandi

Watanabe

et al. 2004

Eur J Immunol

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“…Recently, it was shown that the mast cell content of unstable plaques is increased compared with stable plaques (Kaartinen et al, 1998). Histamine is released from mast cells during myocardial ischemia (Frangogiannis et al, 1998) and is found in significantly higher levels (two-fold increase) in coronary arteries from patients who died from coronary heart disease compared with controls (Kalsner and Richards, 1984).…”

Section: Tg In Atherosclerosismentioning

confidence: 99%

Localization of Tissue Transglutaminase in Human Carotid and Coronary Artery Atherosclerosis: Implications for Plaque Stability and Progression

Haroon

Wannenburg

Gupta

et al. 2001

Laboratory Investigation

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SUMMARY:Although atherosclerosis progresses in an indolent state for decades, the rupture of plaques creates acute ischemic syndromes that may culminate in myocardial infarction and stroke. Mechanical forces and matrix metalloproteinase activity initiate plaque rupture, whereas tissue inhibitors of metalloproteinases have an important (albeit indirect) role in plaque stabilization. In this paper, an enzyme that could directly stabilize the plaque is described. Tissue transglutaminase (TG) catalyzes the formation of ⑀(␥-glutamyl)lysine isopeptide bonds that are resistant to enzymatic, mechanical, and chemical degradation. We performed immunohistochemistry for TG in atherosclerotic human coronary and carotid arteries. TG was most prominent along the luminal endothelium and in the medium of the vessels with a distribution mirroring that of smooth muscle cells. Variable, often prominent, immunoreactivity for TG was also seen in the intima, especially in regions with significant neovascularization. Additionally, TG was detected in fibrous caps and near the "shoulder regions" of some plaques. A monoclonal antibody to the transglutaminase product ⑀(␥-glutamyl)lysine isopeptide demonstrated co-localization with TG antigen. Transglutaminase activity was found in 6 of 14 coronary artery atherectomy samples. Cross-linking of TG substrates such as fibrinogen, fibronectin, vitronectin, collagen type I, and protease inhibitors stabilized the plaque. Furthermore, the activation of transforming growth factor-beta-1 by TG might be an additional mechanism for the promotion of plaque stabilization and progression by increasing the synthesis of extracellular matrix components. (Lab Invest 2001, 81:83-93).

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“…Histamine and other mast cell mediators are known to regulate vasodilation and bronchoconstriction (1,2), and to modulate the functions of other cell types, including monocytes and macrophages (3,4), eosinophils (5,6), T lymphocytes (7), neutrophils (8), and endothelial cells (9). A direct association between mast cell-derived histamine and vascular inflammation is evident from the finding that the coronary arteries of patients with ischemic heart disease contain more mast cells and histamine than normal vessels (10), and patients with variant angina have elevated levels of histamine in the coronary circulation (11). The fact that histamine is able to stimulate endothelial cell production of such proinflammatory cytokines as IL-6 and IL-8 (9,12,13) indicates that this mast cell product can act as an important inflammatory agent in addition to its well-recognized vasoactive functions.…”

mentioning

confidence: 99%

Histamine Directly and Synergistically with Lipopolysaccharide Stimulates Cyclooxygenase-2 Expression and Prostaglandin I2 and E2 Production in Human Coronary Artery Endothelial Cells

Tan

Essengue

Talreja

et al. 2007

The Journal of Immunology

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Although histamine plays an essential role in inflammation, its influence on cyclooxygenases (COX) and prostanoid homeostasis is not well understood. In this study, we investigated the effects of histamine on the expression of COX-1 and COX-2 and determined their contribution to the production of PGE2, prostacyclin (PGI2), and thromboxane A2 in human coronary artery endothelial cells (HCAEC). Incubation of HCAEC monolayers with histamine resulted in marked increases in the expression of COX-2 and production of PGI2 and PGE2 with no significant change in the expression of COX-1. Histamine-induced increases in PGI2 and PGE2 production were due to increased expression and function of COX-2 because gene silencing by small interfering RNA or inhibition of the catalytic activity by a COX-2 inhibitor blocked prostanoid production. The effects of histamine on COX-2 expression and prostanoid production were mediated through H1 receptors. In addition to the direct effect, histamine was found to amplify LPS-stimulated COX-2 expression and PGE2 and PGI2 production. In contrast, histamine did not stimulate thromboxane A2 production in resting or LPS-activated HCAEC. Histamine-induced increases in the production of PGE2 and PGI2 were associated with increased expression of mRNA encoding PGE2 and PGI2 synthases. The physiological role of histamine on the regulation of COX-2 expression in the vasculature is indicated by the findings that the expression of COX-2 mRNA, but not COX-1 mRNA, was markedly reduced in the aortic tissues of histidine decarboxylase null mice. Thus, histamine plays an important role in the regulation of COX-2 expression and prostanoid homeostasis in vascular endothelium.

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Coronary Arteries of Cardiac Patients Are Hyperreactive and Contain Stores of Amines: A Mechanism for Coronary Spasm

Cited by 211 publications

References 12 publications

Inhibition of mast cells by interleukin‐10 gene transfer contributes to protection against acute myocarditis in rats

Inhibition of mast cells by interleukin‐10 gene transfer contributes to protection against acute myocarditis in rats

Localization of Tissue Transglutaminase in Human Carotid and Coronary Artery Atherosclerosis: Implications for Plaque Stability and Progression

Histamine Directly and Synergistically with Lipopolysaccharide Stimulates Cyclooxygenase-2 Expression and Prostaglandin I2 and E2 Production in Human Coronary Artery Endothelial Cells

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