Nitric Oxide Mediates Interleukin-1-Induced Prostaglandin E2 Production by Vascular Smooth Muscle Cells

Inoue, T; Fukuo, Keisuke; Morimoto, Shigeto; Koh, Eitetsu; Ogihara, Toshio

doi:10.1006/bbrc.1993.1836

Cited by 125 publications

(73 citation statements)

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“…The codistribution of iNOS and Cox-2, as was seen in both native and transplant atheroma, has been shown previously in a variety of cell types in vitro, 28 although there is conflicting evidence as to whether NO stimulates 30,31 or inhibits Cox-2 64,65 or whether prostanoids can influence NO output. 65 The finding, however, does allow us to speculate on a direct interaction between eicosanoids and iNOS and/or NO and Cox-2 leading to an exacerbation of the inflammatory process in atherosclerosis.…”

Section: Discussionmentioning

confidence: 77%

“…27 The possibility of significant "cross talk" between NO synthase and Cox has recently been suggested, and colocalization of Cox-2 and iNOS has been demonstrated in animal models of inflammation. 28,29 NO has been shown to enhance Cox activity both in vitro 30,31 and in vivo, 29 and Cox activity can also produce the superoxide anion, 32 thus providing the potential for peroxynitrite formation. It is noteworthy that peroxynitrite may also modulate eicosanoid synthesis, because it has been shown both to activate Cox-2 33 and to inactivate prostacyclin synthase.…”

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confidence: 99%

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Cyclooxygenase-2 Is Widely Expressed in Atherosclerotic Lesions Affecting Native and Transplanted Human Coronary Arteries and Colocalizes With Inducible Nitric Oxide Synthase and Nitrotyrosine Particularly in Macrophages

Baker

Hall

Evans

et al. 1999

ATVB

280

175

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Abstract-Inflammation appears to have a major role in the development of atherosclerotic lesions affecting native and transplanted coronary arteries. The subsequent risk of plaque rupture and acute ischemic events correlates with the degree of inflammation and may be modified by aspirin, an anti-inflammatory cyclooxygenase inhibitor. Cyclooxygenase-2 (Cox-2) and inducible nitric oxide synthase (iNOS) are involved in the inflammatory response via the rapid and exaggerated production of prostanoids and nitric oxide, both of which may have proatherosclerotic effects. These effects may be mediated by the formation of peroxynitrite in the case of nitric oxide and involve "cross talk" between the two enzyme systems. This study aimed to investigate native and transplant atherosclerosis for the presence and distribution of Cox-2 and iNOS. Immunocytochemical studies were performed on atherosclerotic lesions from patients with native (nϭ12) and transplant (nϭ5) coronary disease by using antibodies to Cox-2, iNOS, and nitrotyrosine (an indicator of peroxynitrite production). Control tissue was obtained from unused donor hearts and at the time of autopsy. Cox-2 and iNOS colocalized predominantly in macrophages/foam cells in both types of atherosclerosis. Cox-2 expression was also detected in medial smooth muscle cells and endothelial cells, including those of the vasa vasorum. Nitrotyrosine was found in the same distribution as that of iNOS and was colocalized with Cox-2 in macrophages. Cox-2 and iNOS are coexpressed in native and transplant atherosclerosis, possibly allowing for interaction between the enzymes and suggesting an alternative mechanism for the benefits of aspirin via inhibition of Cox-2 activity.

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Section: Discussionmentioning

confidence: 77%

mentioning

confidence: 99%

Cyclooxygenase-2 Is Widely Expressed in Atherosclerotic Lesions Affecting Native and Transplanted Human Coronary Arteries and Colocalizes With Inducible Nitric Oxide Synthase and Nitrotyrosine Particularly in Macrophages

Baker

Hall

Evans

et al. 1999

ATVB

280

175

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“…27 The co-induction of COX-2 and iNOS has also been observed in studies in vitro of rat vascular smooth muscle cells, 28,29 glomerular mesangial cells, 7 murine macrophages, 30 rat islets of Langerhans, 31 human endothelial cells, 32 articular chondrocytes, 33 and rabbit hepatocytes 34 incubated with endotoxin and/or cytokines but not in similar studies of human fetal cell fibroblasts 6 or bovine aortic endothelial cells. 35 Proinflammatory cytokines known to be synthesized and released by T lymphocytes and macrophages during cardiac allograft rejection are probably responsible for induction of COX-2 in this situation.…”

Section: Discussionmentioning

confidence: 88%

“…In cultured bovine endothelial cells, NO or NO donor drugs have been shown to inhibit PGI 2 release by bradykinin (COX-1) 39 and to inhibit COX-2 induction and activity in rat Kupffer cells. 34 In contrast, however, NO and NO donor drugs have been shown to stimulate COX-1 and COX-2 activity in endotoxin-activated murine macrophages 6 and in vascular smooth muscle cells 28 and human endothelial cells. 39,40 Similarly, in the hydronephrotic model of renal inflammation, 22 in air-pouchinduced inflammation, 24 there is evidence that NO augments the activity of COX-1 and COX-2, leading to enhanced synthesis of prostaglandins.…”

Section: Discussionmentioning

confidence: 98%

Upregulation of COX-2 During Cardiac Allograft Rejection

Yang

Szabolcs

et al. 2000

Circulation

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Background-The hypothesis that cyclooxygenase-2 (COX-2) is involved in the myocardial inflammatory response during cardiac allograft rejection was investigated using a rat heterotopic abdominal cardiac transplantation model. Methods and Results-COX-2 mRNA and protein in the myocardium of rejecting cardiac allografts were significantly elevated 3 to 5 days after transplantation compared with syngeneic controls (nϭ3, PϽ0.05). COX-2 upregulation paralleled in time and extent the upregulation of iNOS mRNA, protein, and enzyme activity in this model. COX-2 immunostaining was prominent in macrophages infiltrating the rejecting allografts and in damaged cardiac myocytes. Prostaglandin (PG) levels in rejecting allografts were also higher than in native hearts. Because NO has been reported to modulate PG synthesis by COX-2, additional transplants were performed using animals treated with a selective COX-2 inhibitor (SC-58125) and a selective inhibitor of the inducible nitric oxide synthase (iNOS) N-aminomethyl-L-lysine. At posttransplant day 5, inhibitor administration resulted in a significant reduction of COX-2 mRNA expression (3764Ϯ337 versus 5110Ϯ141 arbitrary units, nϭ3, PϽ0.05) and iNOS enzymatic activity (1.7Ϯ0.4 versus 22.8Ϯ14.4 nmol/mg protein, nϭ3, PϽ0.01) compared with vehicle-treated allogeneic transplants. Allograft survival in treated animals was increased modestly from 5.4 to 6.4 days (PϽ0.05). However, apoptosis of cardiac myocytes (TUNNEL method) was only marginally reduced relative to vehicle controls in treated graft recipients. The intensity of allograft rejection was also similar in the treated and untreated allografts. Conclusions-The data indicates that COX-2 expression is enhanced in parallel with iNOS in the myocardium during cardiac allograft rejection. (Circulation. 2000;101:430-438.)

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“…VSMC were extracted from the thoracic aorta of WKY and SHR rats and cultured as described by Inoue et al [10].…”

Section: Cell Culturementioning

confidence: 99%

Decreased l‐arginine‐nitric oxide pathway in cultured myoblasts from spontaneously hypertensive versus normotensive Wistar‐Kyoto rats

Morvan-Dubois

1996

FEBS Letters

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The hypertrophy of the arterial media exhibited by spontaneously hypertensive rats is related to the hyperproliferation of their smooth muscle cells in culture. Using two methods to assay nitric oxide synthase activity, we showed that this abnormal proliferation results from a decreased activity of the inducible NOS II and less modulation of this enzymatic activity by these cells compared to control Wistar Kyoto cells.

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Nitric Oxide Mediates Interleukin-1-Induced Prostaglandin E2 Production by Vascular Smooth Muscle Cells

Cited by 125 publications

References 0 publications

Cyclooxygenase-2 Is Widely Expressed in Atherosclerotic Lesions Affecting Native and Transplanted Human Coronary Arteries and Colocalizes With Inducible Nitric Oxide Synthase and Nitrotyrosine Particularly in Macrophages

Cyclooxygenase-2 Is Widely Expressed in Atherosclerotic Lesions Affecting Native and Transplanted Human Coronary Arteries and Colocalizes With Inducible Nitric Oxide Synthase and Nitrotyrosine Particularly in Macrophages

Upregulation of COX-2 During Cardiac Allograft Rejection

Decreased l‐arginine‐nitric oxide pathway in cultured myoblasts from spontaneously hypertensive versus normotensive Wistar‐Kyoto rats

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