Cultured endothelial cells synthesize both platelet-activating factor and prostacyclin in response to histamine, bradykinin, and adenosine triphosphate.

McIntyre, Thomas M.; Zimmerman, Guy A.; Satoh, Kei; Prescott, Stephen M.

doi:10.1172/jci111957

Cited by 423 publications

(180 citation statements)

References 33 publications

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“…The present finding that histamine-induced COX-2 expression and PGI 2 production are inhibited by the H 1 R antagonist, fexofenidine, and not by the H 2 R antagonist, famotidine, suggests that histamine-mediated prostanoid homeostasis in HCAEC is regulated via H 1 R activation. These findings are in agreement with our previous reports demonstrating a distinct role of H 1 R in histamine-mediated proinflammatory cytokine production and TLR expression (16) and of others on histamine-induced released of PGI 2 in HUVECs (32,33). It should be noted that the stimulatory effect of histamine on COX-2 expression is not always mediated via H 1 R, but is rather dependent on the cell type.…”

Section: Figuresupporting

confidence: 93%

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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Section: Figuresupporting

confidence: 93%

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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“…Maximal inhibition of the early phase of leakage was approximately 50% and included doses of WEB 2086 which we have shown to block completely equivalent PAF-induced leakage . Similarly, inhibition approached 50% at a dose of BN 52021 shown previously to inhibit markedly PAFinduced bronchoconstriction (Braquet et al, 1985 (McIntyre et al, 1985) and bovine aorta (Stewart et al, 1989). …”

Section: Discussionmentioning

confidence: 59%

Bradykinin‐induced plasma exudation in guinea‐pig airways: involvement of platelet activating factor

Rogers

Dijk

Barnes

1990

British J Pharmacology

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1 We studied the effect of bradykinin on plasma exudation in the airways of the anaesthetized guineapig in vivo. Tissue content of extravasated Evans blue dye was used as an index of protein exudation in the larynx, trachea, main bronchi and intrapulmonary airways (i.p.a.). 2 Bradykinin increased the content of Evans blue in all tissues studied in a dose-related manner. The response was greatest in the main bronchi and i.p.a., less in the trachea and least in the larynx. A dose of 47 nmol kg-1 was the lowest tested which caused significant (P < 0.001) plasma exudation with increases in leakage above control values of 256% in the larynx, 405% in the trachea, 394% in the main bronchi and 485% in intrapulmonary airways. 3 Leakage was significantly (P < 0.05) increased above control values by 1 min after bradykinin (47nmol kg-1) in the main bronchi and intrapulmonary airways and was maximal in all airways 5min after bradykinin. Although reduced by 15min, the tissue content of dye was still significantly (P < 0.05) increased 2 h after bradykinin. 4 The prolonged tissue dye retention was due to a later phase of slow and maintained exudation preventing full clearance of dye after the initial response. 5The initial phase of leakage was partially attenuated by the platelet activating factor (PAF) receptor antagonists WEB 2086 or BN 52021, by indomethacin or by inhibiting sensory nerve activation by opioid anaesthesia: it was not affected by mepyramine and cimetidine nor by the sulphidopeptide leukotriene receptor antagonists FPL 55712 or ICI 198,615. Adrenoceptor blockade of the anti-leakage effects of endogenously-released catecholamines significantly (P < 0.05) enhanced leakage. 6 The later phase of plasma leakage was completely inhibited by the PAF antagonists. 7 We conclude that, in guinea-pig airways in vivo, the initial phase of bradykinin-induced plasma exudation is mediated in part by PAF, sensory nerves and prostaglandins, whereas the later, prolonged phase of leakage is mediated exclusively by PAF. If bradykinin is generated in asthma, its potent and prolonged effects on plasma leakage may contribute significantly to airway oedema and may be involved in the development of bronchial hyperresponsiveness.

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“…BK, consisting of nine amino acids, is a major kinin with welldocumented pharmacological properties including vasodilatation and vascular leakage. It enhances production of prostaglandins, leukotrienes, and platelet-activating factor in endothelial cells and fibroblasts [24,25].…”

Section: Discussionmentioning

confidence: 99%

Bradykinin stimulates IL-6 and IL-8 production by human lung fibroblasts through ERK- and p38 MAPK-dependent mechanisms

Hayashi¹,

Yamashita

Matsui

et al. 2000

Eur Respir J

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Bradykinin (BK) is a major kinin with well-documented pharmacological properties including vascular leakage and induction of a variety of cytokines. However, the intracellular signalling mechanisms by which BK induced proinflammatory cytokine production have not been fully elucidated. This study investigated the role of the extracellular signal-regulated protein kinase 1/2 (ERK 1/2) and p38 mitogen-activated protein kinase (p38 MAPK) in the BK-induced interleukin (IL)-6 and IL-8 production by human lung fibroblasts.Lung fibroblasts were stimulated with BK in the presence or in the absence of PD98059, a specific MAPK/ERK kinase-1 inhibitor, or SB203580, a specific p38 MAPK inhibitor, and IL-6 or IL-8 production and their gene expression was examined. BK-induced ERK 1/2 or p38 MAPK phosphorylation was also analysed by Western blot analysis.BK at nanomolar concentrations stimulated lung fibroblasts to produce IL-6 and IL-8 along with increased ERK 1/2 and p38 MAPK phosphorylation. BK-induced IL-6 and IL-8 synthesis was inhibited by a B2-type BK receptor antagonist. Furthermore, PD98059 or SB203580 significantly suppressed BK-induced IL-6 and IL-8 production and their gene expression.These results indicate that bradykinin-induced interleukin-6 and interleukin-8 production are at least partly mediated through the extracellular signal-related protein kinase 1/2 and p38 mitogen-activated protein kinase pathway-dependent activation in human lung fibroblasts, and suggest that bradykinin appears to be involved in the inflammatory reaction leading to acute lung injury through stimulating interleukin-6 and interleukin-8 production by lung fibroblasts. Eur Respir J 2000; 16: 452±458.

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Cultured endothelial cells synthesize both platelet-activating factor and prostacyclin in response to histamine, bradykinin, and adenosine triphosphate.

Cited by 423 publications

References 33 publications

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

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

Bradykinin‐induced plasma exudation in guinea‐pig airways: involvement of platelet activating factor

Bradykinin stimulates IL-6 and IL-8 production by human lung fibroblasts through ERK- and p38 MAPK-dependent mechanisms

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