Endothelin-1 enhances superoxide generation of human neutrophils stimulated by the chemotactic peptide n-formyl-methionyl-leucyl-phenylalanine

Ishida, Kiyoshi; Takeshige, Koichiro; Minakami, Shigeki

doi:10.1016/s0006-291x(05)80061-0

Cited by 116 publications

(54 citation statements)

References 20 publications

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“…Although we did not measure phospholipase D activity in alveolar macrophages, ET-1 has been reported to activate phospholipase D in cultured vascular smooth muscle cells (Konishi et al, 1991), which possess predominantly ETA receptors (Hosoda et al, 1991). It is worth mentioning that similar potentiation by ET-1 of f-Met-Leu-Phe-induced superoxide formation has been reported for human neutrophil granulocytes (Ishida et al, 1990).…”

Section: Discussionmentioning

confidence: 66%

Acute pro‐inflammatory actions of endothelin‐1 in the guinea‐pig lung: involvement of ET_A and ET_B receptors

Filep

Fournier

Földes-Filep

1995

British J Pharmacology

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1 Although recent observations suggest that endothelin-l (ET-1) may play a role in the pathogenesis of asthma, to date little is known about the effects of ET-1 on parameters other than bronchoconstriction. The objectives of the present experiments were to study whether intravenously administered ET-1 could exert pro-inflammatory actions in the guinea-pig lung and to assess the involvement of endothelin ETA and ETB receptors in these events by using the ETA receptor-selective antagonist, FR 139317, the novel ETA/ETB receptor antagonist, bosentan and the ETB receptor-selective agonist, IRL 1620. 2 Bolus i.v. injection of ET-1 (0.1-1 nmol kg-') to anaesthetized guinea-pigs evoked dose-dependent increases in mean arterial blood pressure which lasted for 6-12 min. This was accompanied by a dose-dependent haemoconcentration (8-15% plasma volume losses) and increases (up to 546%) in albumin extravasation in the trachea, upper and lower bronchi, but not in the pulmonary parenchyma. Qualitatively similar changes were observed following i.v. injection of the ETB receptor agonist, IRL 1620 (0.3 and 1 nmol kg-'), although IRL 1620 appeared to be about 3 times less potent than ET-1. The ETA receptor-selective antagonist, FR 139317 (2.5 mg kg-') inhibited the ET-1 (1 nmol kg-')-induced pressor response, haemoconcentration and albumin extravasation by 75, 77 and 60-70%, respectively, whereas it did not attenuate IRL 1620 (1 nmol kg-')-induced changes. The ETA/ETB receptor antagonist, bosentan (10mgkg-') almost completely inhibited the pressor, haemoconcentration and permeability effects of both ET-I and IRL 1620. 3 ET-1, but not IRL 1620 (0.1-1 nmol kg-1), produced a dose-dependent neutropenia with relative lymphocytosis and monocytosis, but did not induce influx of neutrophil granulocytes into pulmonary tissues or the bronchoalveolar space. ET-1 (1 nmol kg-')-induced neutropenia was prevented by pretreatment of the animals with FR 139317 (2.5 mg kg-'), bosentan (10 mg kg-') or adrenaline (90 nmol kg-'), indicating that ET-1 caused intravascular sequestration of neutrophil granulocytes. 4 ET-1 or IRL 1620 (10-II_ 10-6 M) alone did not activate alveolar macrophages in vitro, whereas at a concentration of 10-8 M, ET-1, but not IRL 1620, markedly potentiated superoxide production in response to f-Met-Leu-Phe (10-9-10-7 M) and platelet-activating factor (PAF, 10-9-10-7 M), but not to phorbol 12-myristate 13-acetate (10-9 M). ET-1 did not affect f-Met-Leu-Phe-or PAF-induced increases in intracellular free calcium concentration. This potentiating effect of ET-1 was abolished by FR 139317 (1.5 X 10-7 M). 5 We conclude that, in addition to evoking airway contractions, ET-1 exerts pro-inflammatory actions via activation of the ETA and to a lesser extent the ETB receptors, and therefore, might contribute to the airway inflammation present in asthma. These findings also suggest the therapeutic potential of ETA/ETB receptor and perhaps ETA receptor-selective antagonists in this disease.

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Section: Discussionmentioning

confidence: 66%

Acute pro‐inflammatory actions of endothelin‐1 in the guinea‐pig lung: involvement of ET_A and ET_B receptors

Filep

Fournier

Földes-Filep

1995

British J Pharmacology

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“…It induces the expression of membrane-associated markers, the release of fibronectin [36] and the secretion of oxygen radicals by normal human alveolar macrophages [35]. ET-1 also acts on the neutrophil to induce its aggregation [37], promote its adhesion to endothelial cells through the expression of membrane adhesion molecules [38] and to enhance its superoxide generation [39]. ET-1 could act also as an immunoregulatory peptide through its action on nonimmune cells.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia reduces endothelin production by rat alveolar type II cells in primary culture

Crestani

Odoux²,

Rolland³

et al. 1998

Eur Respir J

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Type II alveolar epithelial cells (ATII cells) have been shown to play a key role in the regulation of the alveolar space. ATII cells synthesize and secrete surfactant, control the volume and composition of the epithelial lining fluid and proliferate and differentiate into type I alveolar epithelial cells after injury in order to maintain the integrity of the alveolar wall. Moreover, ATII cells are ideally located to have a role in modulating the activation or proliferation state of macrophages, fibroblasts or endothelial cells, because of the close proximity of the cell types in the alveolar space.The interactions between the alveolar epithelial cells and the other cells located in the alveoli are brought about by the secretion of mediators such as cytokines [1], but other mediators are probably involved in this phenomenon. Among these mediators, endothelin (ET)-1 a 21 amino acid peptide may play an important role. Indeed, beside its potent effect on the constriction of vascular and bronchial smooth muscle cells, ET-1 acts as a mitogen for different cell types, such as fibroblasts or smooth muscle cells [2]. ET-1 is also involved in the modulation of the inflammatory response through a direct effect on alveolar macrophages [3] or mastocytes [4].It has been shown that hyperplastic alveolar epithelial cells express preproendothelin-1 (preproET-1) messenger ribonucleic acid (mRNA) and immunoreactive ET (irET)-1 in the human fibrotic lung [5], although conflicting data exist [6]. Rat ATII cells in primary culture [7], and a cell line derived from rat ATII cells, have been shown to secrete ET-1 in vitro [8].Hypoxia has been identified as an important modulator of ET-1 production by endothelial cells. Hypoxia increases ET-1 production by human umbilical vein endothelial cells [9], but decreases ET-1 production by rat lung endothelial cells [10]. The effect of hypoxia on ET-1 production by rat ATII cells has never been evaluated, despite the fact that ATII cells are potential targets for hypoxia in the alveolar space both in physiological (high altitude) and pathological (e.g. lung parenchyma consolidation) conditions. Therefore, the aims of this study were: 1) to characterize the regulation of ET-1 production by rat ATII cells in primary culture under low oxygen tension; and 2) to evaluate the influence of nitric oxide on ET-1 production by rat ATII cells. Materials and methods ReagentsTissue culture media and foetal bovine serum were obtained from Gibco BRL Life Technologies (Cergy Pontoise, Hypoxia reduces endothelin production by rat alveolar type II cells in primary culture. B. Crestani, C. Odoux, C. Rolland, F. Moldovan, P. Cornillet, J. Fiet, M. Aubier. ©ERS Journals Ltd 1998. ABSTRACT: The purpose of the study was to describe endothelin (ET) production and to characterize the effect of hypoxia on preproendothelin-1 (preproET-1) messenger ribonucleic acid (mRNA) expression and ET secretion by rat type II pneumocytes in vitro.Rat type II pneumocytes were incubated in a sealed chamber containing a normoxic (21% ...

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“…It is known that oxidant stress reduces NO bioavailability, contributing to endothelial dysfunction in patients with atherosclerosis and its risk factors. 40,41 ET-1-stimulated production of oxygen free radicals by neutrophils in vitro is inhibited by ET A receptor blockade, 42,43 and postischemic coronary endothelial dysfunction can be attenuated by pretreatment with BQ-123. 44 Thus, reduced oxidative consumption of endothelium-derived NO provides a compelling explanation for our findings.…”

Section: Potential Mechanismsmentioning

confidence: 99%

Coronary Vasodilation and Improvement in Endothelial Dysfunction With Endothelin ET _A Receptor Blockade

Halcox

Nour

Zalos

et al. 2001

Circulation Research

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Abstract-The endothelium-derived peptide endothelin-1 (ET-1) causes vasoconstriction predominantly via smooth muscle ET A receptor activation. We hypothesized that ET A receptor inhibition would improve human coronary vascular function. We studied unobstructed coronary arteries of 44 patients with atherosclerosis or its risk factors. Epicardial diameter (D) Key Words: endothelin Ⅲ coronary circulation Ⅲ endothelial function Ⅲ atherosclerosis E ndothelin (ET), a powerful vasoconstrictor peptide, exists in 3 isoforms, ET-1, ET-2, and ET-3. 1,2 ET-1, the predominant isopeptide released from endothelial cells, is likely to be physiologically the most important in regulating vascular function via its action on 2 distinct receptor subtypes, ET A and ET B . 3 The ET A receptor has a high affinity for ET-1, is selectively expressed on vascular smooth muscle cells, and is the predominant ET receptor in the heart, 4,5 whereas the ET B receptor has equal affinity for all 3 isoforms of ET and is present on both endothelial and vascular smooth muscle cells. 6 ET-1, via stimulation of ET A receptors on vascular smooth muscle cells, activates phospholipase C, resulting in generation of inositol triphosphate, intracellular calcium accumulation, and vasoconstriction. 4,7,8 ET-1 levels are elevated in conditions associated with vascular endothelial dysfunction such as hyperlipidemia, hypertension, smoking, heart failure, and atherosclerosis, suggesting a possible pathophysiological role of ET-1 in these conditions. 9 -14 However, as ET-1 is preferentially secreted abluminally by the endothelial cells, circulating levels appear not to accurately reflect the vascular activity of ET-1, thus necessitating the use of selective antagonists to characterize its physiological effects. 15 ET A receptor antagonism vasodilates the forearm microcirculation of healthy volunteers and subjects with hypertension, heart failure, and hyperlipidemia, suggesting that endogenous ET-1 regulates resting peripheral vascular tone in humans. 16 -21 Endogenous ET-1 acting via the ET A receptor contributes toward the maintenance of coronary vasoconstrictor tone. [22][23][24] Although chronic ET A receptor blockade attenuated the progression of endothelial vasomotor dysfunction in animal models, 25,26 whether endogenous ET-1 contributes toward endothelial dysfunction in the human coronary circulation in vivo is unknown.We hypothesized that ET-1 activity may contribute to both the resting coronary vasomotor tone and the endothelial dysfunction observed in the coronary circulation of patients with atherosclerosis. Therefore, in this study, we investigated the effect of ET A receptor antagonism on coronary vasomotor function and on transcardiac ET-1 uptake in patients with and without coronary atherosclerosis.

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Endothelin-1 enhances superoxide generation of human neutrophils stimulated by the chemotactic peptide n-formyl-methionyl-leucyl-phenylalanine

Cited by 116 publications

References 20 publications

Acute pro‐inflammatory actions of endothelin‐1 in the guinea‐pig lung: involvement of ET_A and ET_B receptors

Acute pro‐inflammatory actions of endothelin‐1 in the guinea‐pig lung: involvement of ET_A and ET_B receptors

Hypoxia reduces endothelin production by rat alveolar type II cells in primary culture

Coronary Vasodilation and Improvement in Endothelial Dysfunction With Endothelin ET _A Receptor Blockade

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Endothelin-1 enhances superoxide generation of human neutrophils stimulated by the chemotactic peptide n-formyl-methionyl-leucyl-phenylalanine

Cited by 116 publications

References 20 publications

Acute pro‐inflammatory actions of endothelin‐1 in the guinea‐pig lung: involvement of ETA and ETB receptors

Acute pro‐inflammatory actions of endothelin‐1 in the guinea‐pig lung: involvement of ETA and ETB receptors

Hypoxia reduces endothelin production by rat alveolar type II cells in primary culture

Coronary Vasodilation and Improvement in Endothelial Dysfunction With Endothelin ET A Receptor Blockade

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Acute pro‐inflammatory actions of endothelin‐1 in the guinea‐pig lung: involvement of ET_A and ET_B receptors

Acute pro‐inflammatory actions of endothelin‐1 in the guinea‐pig lung: involvement of ET_A and ET_B receptors

Coronary Vasodilation and Improvement in Endothelial Dysfunction With Endothelin ET _A Receptor Blockade