Angiotensin II is chemotactic for a T-cell subset which can express migration inhibition factor activity in murine schistosomiasis mansoni

Weinstock, Joel V.; Blum, Arthur M.; Kassab, Joseph

doi:10.1016/0008-8749(87)90278-4

Cited by 33 publications

(18 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, Ang II may contribute to the development of an acute coronary syndrome through the migration of macrophages into a neointimal area 33 or by producing reactive oxygen species and thereby increasing oxidative stress. 34 Increased secretion of macrophage-derived interleukins was observed in cells exposed to oxidative stress, such as oxidized LDL or cellular lipid peroxidation induced by iron ions.…”

Section: Discussionmentioning

confidence: 99%

Expression of Angiotensin II and Interleukin 6 in Human Coronary Atherosclerotic Plaques

et al. 2000

View full text Add to dashboard Cite

Background-Patients with an activated renin-angiotensin system (RAS) or genetic alterations of the RAS are at increased risk of myocardial infarction (MI). Administration of ACE inhibitors reduces the risk of MI, and acute coronary syndromes are associated with increased interleukin 6 (IL-6) serum levels. Accordingly, the present study evaluated the expression of angiotensin II (Ang II) in human coronary atherosclerotic plaques and its influence on IL-6 expression in patients with coronary artery disease. Methods and Results-Immunohistochemical colocalization of Ang II, ACE, Ang II type 1 (AT 1 ) receptor, and IL-6 was examined in coronary arteries from patients with ischemic or dilated cardiomyopathy undergoing heart transplantation (nϭ12), in atherectomy samples from patients with unstable angina (culprit lesion; nϭ8), and in ruptured coronary arteries from patients who died of MI (nϭ13). Synthesis and release of IL-6 was investigated in smooth muscle cells and macrophages after Ang II stimulation. Colocalization of ACE, Ang II, AT 1 receptor, and IL-6 with CD68-positive macrophages was observed at the shoulder region of coronary atherosclerotic plaques and in atherectomy tissue of patients with unstable angina. Ang II was identified in close proximity to the presumed rupture site of human coronary arteries in acute MI. Ang II induced synthesis and release of IL-6 shortly after stimulation in vitro in macrophages and rat smooth muscle cells. Conclusions-Ang II, AT 1 receptor, and ACE are expressed at strategic sites of human atherosclerotic coronary arteries, suggesting that Ang II is produced primarily by ACE within coronary plaques. The observation that Ang II induces IL-6 and their colocalization with the AT 1 receptor and ACE is consistent with the notion that the RAS may contribute to inflammatory processes within the vascular wall and to the development of acute coronary syndromes. (Circulation. 2000;101:1372-1378.)Key Words: interleukins Ⅲ angiotensin Ⅲ angina Ⅲ myocardial infarction Ⅲ arteries Ⅲ receptors R upture of atherosclerotic plaques occurs predominantly at the edges of the plaque's fibrous cap, the shoulder region, that is, areas of accumulated inflammatory cells, for example, macrophages, T-lymphocytes, and mast cells in close proximity to vascular smooth muscle cells (SMC). [1][2][3][4][5][6] The activated inflammatory cells stimulate their neighboring cells to erode the extracellular matrix through the release of inflammatory cytokines. The decay of the framework that forms the plaque cap leads to plaque rupture 1,7,8 and resembles the morphological correlate of an acute coronary syndrome. Serum levels of interleukin 6 (IL-6) are increased in patients with unstable angina 9 and may trigger the onset of an acute coronary syndrome. 10 IL-6 is known to be involved in the stimulation of matrix-degrading enzymes, for example, metalloproteinases. 11In parallel, the renin-angiotensin system (RAS) has been suggested to be involved in the development of acute coronary syndromes, based on the observat...

show abstract

Section: Discussionmentioning

confidence: 99%

Expression of Angiotensin II and Interleukin 6 in Human Coronary Atherosclerotic Plaques

et al. 2000

View full text Add to dashboard Cite

show abstract

“…In addition to its effects on cardiovascular pathology such as arterial hypertension, left ventricular hypertrophy, and restenosis (Suzuki et al, 2000;Ruiz-Ortega et al, 2001;Phillips and Kagiyama, 2002), Ang II may initiate the inflammatory process (Suzuki et al, 2003). For example, Ang II contributes to the recruitment of inflammatory cells into tissue through the regulation of adhesion molecules and chemokines and by directly activating chemotaxis (Suzuki et al, 2000;Ruiz-Ortega et al, 2001;Phillips and Kagiyama, 2002;Riaz et al, 2004) in a variety of cell types including monocytes (Ni et al, 2004), vascular smooth muscle cells (Meloche et al, 2000), neonatal cardiac fibroblasts (Graf et al, 2000), retinal pericytes (Nadal et al, 2002), T cells (Weinstock et al, 1987), and neutrophils (Elferink and de Koster, 1997). A prototypical GPCR, AT 1 R signaling is generally dependent on heterotrimeric G-proteins and is known to be primarily coupled to G ␣q/11 and in some circumstances to G ␣i and G ␣o (de Gasparo et al, 2000;Touyz and Schiffrin, 2000;Berk, 2001).…”

mentioning

confidence: 99%

β-Arrestin 2-Dependent Angiotensin II Type 1A Receptor-Mediated Pathway of Chemotaxis

Hunton

Barnes²,

Kim³

et al. 2005

Mol Pharmacol

113

126

View full text Add to dashboard Cite

“…Cet enzyme a comme fonction principale d'effectuer la conversion de l'angiotensine I en angiotensine II dans le système rénine-angiotensine (Erdos, 1977), système de régulation de la pression corporelle. L'hypothèse serait que ACE aurait un effet chémotactique sur les lymphocytes T via l'angiotensine II (voir figure 2b) (Weinstock et al, 1987). Pour ce qui est des maladies cardiovasculaires, selon l'équipe de Diet , ACE serait présent dans les plaques athérosclérotiques, plus particulièrement dans la section de haute vascularisation {shoulder region) à l'endroit où on retrouve un regroupement de lymphocytes T et de macrophages, et participerait probablement à la croissance de la plaque .…”

Section: Enzyme De Conversion De Vangiotensineunclassified

Distribution géographique de certains polymorphismes associés à des maladies inflammatoires chroniques dans les régions administratives du Québec /

Madore¹

2005

View full text Add to dashboard Cite

Angiotensin II is chemotactic for a T-cell subset which can express migration inhibition factor activity in murine schistosomiasis mansoni

Cited by 33 publications

References 20 publications

Expression of Angiotensin II and Interleukin 6 in Human Coronary Atherosclerotic Plaques

Expression of Angiotensin II and Interleukin 6 in Human Coronary Atherosclerotic Plaques

β-Arrestin 2-Dependent Angiotensin II Type 1A Receptor-Mediated Pathway of Chemotaxis

Distribution géographique de certains polymorphismes associés à des maladies inflammatoires chroniques dans les régions administratives du Québec /

Contact Info

Product

Resources

About