Activation of Guinea Pig Alveolar Macrophages by Endothelin-1

Millul, Valerie; Lagente, Vincent; Gillardeaux, O.; Boichot, Elisabeth; Dugas, B.; Menciahuerta, Jm; Béréziat, G.; Braquet, P.; Masliah, J.

doi:10.1097/00005344-199100177-00067

Cited by 27 publications

(7 citation statements)

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“…It was reported that ET‐1 increases intracellular Ca 2+ in macrophages, 34 which causes an increase in the production of cytokines 28,35 and superoxide anion 36 in macrophages. It has been reported that ET B receptors, but not ET A receptors, are expressed in rat peritoneal macrophages in vitro.…”

Section: Discussionmentioning

confidence: 99%

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Corresponding distributions of increased endothelin‐B receptor expression and increased endothelin‐1 expression in the aorta of apolipoprotein E‐deficient mice with advanced atherosclerosis

Kobayashi

Miyauchi

Iwasa³

et al. 2000

Pathology International

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Endothelin (ET)-1 causes proliferation of vascular smooth muscle cells (VSMC). Although it has been reported that stimulation of ET(B) receptors as well as ET(A) receptors promote proliferation of VSMC, the precise distribution of each receptor subtype in atherosclerotic vessels is unknown. Previous studies demonstrated that apolipoprotein E (apoE)-deficient mice have hypercholesterolaemia and develop severe atherosclerosis. To investigate the pathophysiological roles of vascular ET system in atherosclerosis, we examined preproET-1 messenger ribonucleic acid expression in the aorta of apoE-deficient mice, and performed immunohistochemical staining for ET-1 and each ET receptor subtype (ET(A) and ET(B) receptors) in the atherosclerotic lesions of these mice. The level of preproET-1 mRNA in the aorta was significantly higher in the apoE-deficient mice than in the control mice. Strong ET-1 staining was observed in the macrophage-foam cells, intimal and medial VSMC in the atherosclerotic lesions of the apoE-deficient mice. In addition, in the atherosclerotic lesions, strong ET(B) receptor staining was observed in the macrophage-foam cells, intimal and medial VSMC, which distribution corresponded closely to that of ET-1. ET(A) receptor staining was observed in the medial VSMC of both groups, but not in the macrophage-foam cells of the apoE-deficient mice. ET(A) receptor staining in the medial VSMC was stronger in the apoE-deficient mice than in the control mice. These results suggest that the vascular ET system, including ET-1 and ET receptors, is activated in the atherosclerotic lesions of apoE-deficient mice. Since the distribution of strong ET(B) receptor staining corresponded closely to that of ET-1, it is suggested that the ET system, mediated by ET(B) receptors, has an important role in the pathophysiology of the atherosclerotic lesions of apoE-deficient mice.

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Section: Discussionmentioning

confidence: 99%

“…26,27 In addition, ET-1 can increase the production of cytokines, which also induces proliferation of VSMC, in macrophages. 28 Thus, in apoE-deficient mice, enhanced ET-1 production in the VSMC and macrophage-foam cells of atherosclerotic lesions may accelerate the progression of atherosclerosis.…”

Section: Et-1 and Atherosclerosismentioning

confidence: 99%

Corresponding distributions of increased endothelin‐B receptor expression and increased endothelin‐1 expression in the aorta of apolipoprotein E‐deficient mice with advanced atherosclerosis

Kobayashi

Miyauchi

Iwasa³

et al. 2000

Pathology International

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“…2 Vigne and Frelin 56 suggested that release of arachidonic acid through the activation of phospholipase A 2 in brain capillary endothelial cells by ET-1 may play a role in the development of delayed cerebral vasospasm following SAH. In a study by Millul, et al, 38 ET-1 (0.1-10 nM) induced concentration-and time-dependent release of thromboxane B 2 , the stable metabolite of thromboxane A 2 , from guinea pig alveolar macrophages, indicating also that ET-1 activates release of metabolites of arachidonic acid through phospholipase A 2 .…”

Section: Endothelin-1 Synthesis and Functionmentioning

confidence: 97%

“…52 Endothelin may also induce liberation of arachidonic acid metabolites (vasoconstrictive prostaglandins from the endothelium and thromboxane from platelets) through activation of phospholipase A 2 . 38,56 Platelet thromboxane release may be important in development of vasospasm during the 1st week after aneurysmal SAH. 22,24 Hypertension, Cigarette Smoking, and Vasospasm Hypertension has been shown to increase, independently from other factors, the risk of cerebral infarction after SAH.…”

Section: Mechanism Of Et-1-induced Post-sah Vasospasmmentioning

confidence: 99%

Plasma endothelin concentrations after aneurysmal subarachnoid hemorrhage

Juvela

2000

Journal of Neurosurgery

121

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Endothelin concentrations seem to correlate with delayed cerebral ischemia and vasospasm after SAH. The highest levels of ET are predictive of the symptoms of cerebral ischemia and vasospasm, and ET may also worsen ischemia in patients with a history of hypertension. Thus, ET may be an important causal or contributing factor to vasospasm, but its significance in the pathogenesis of vasospasm remains unknown.

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“…A better understanding of the regulation of the production of this peptide in the pulmonary system is of interest since ET‐1 has been implicated in various physiological and pathological functions (reviewed by Battistini et al 1993). These include (1) modulating chloride secretion by tracheal epithelial cells (Plews et al ., 1991; Satoh et al ., 1992), (2) promoting mitogenesis of airway smooth muscle cells (Noveral et al ., 1992; Glassberg et al ., 1994), (3) inducing activation of alveolar macrophages, that subsequently increase eicosanoid release (Millul et al ., 1991), and (4) increasing superoxide production (Haller et al ., 1991). Moreover, ET‐1 is recognized as a potent constrictor of airway smooth muscle (Inui et al ., 1994) that has been implicated in pulmonary hypertension (Uchida et al ., 1988; Cernacek & Stewart, 1989; Horgan et al ., 1991), asthma (Boichot et al ., 1991) and cystic fibrosis (Plews et al ., 1991).…”

Section: Introductionmentioning

confidence: 99%

Adenosine induces cyclic‐AMP formation and inhibits endothelin‐1 production/secretion in guinea‐pig tracheal epithelial cells through A_2B adenosine receptors

Pelletier

Dubé

Villeneuve

et al. 2000

British J Pharmacology

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1 The adenosine receptor subtype mediating adenosine 3' : 5'-cyclic monophosphate (cyclic AMP) formation and the e ect of its activation on endothelin-1 (ET-1) secretion were studied in primary cultures of tracheal epithelial cells. 2 Adenosine analogues showed the following rank order of potency (pD 2 value) and intrinsic activity on the generation of cyclic AMP by tracheal epithelial cells: 5'-N-ethylcarboxyamidoadenosine (NECA, A 1 /A 2A /A 2B , pD 2 : 5.44+0.16)4adenosine (ADO, non selective, pD 2 : 4.99+0.09; 71+9% of NECA response) 52-Cl-adenosine (2CADO, non selective, pD 2 : 4.72+0.14; 65+9% of NECA response)444CGS21680 (A 2A ; inactive at up to 100 mM). 3 Cyclic AMP formation stimulated by NECA in guinea-pig tracheal epithelial cells was inhibited by adenosine receptor antagonist with the following order of apparent a nity (pA 2 value): Xanthine amine congeners (XAC, A 2A /A 2B , 7.89+0.22)4CGS15943 (A 2A /A 2B , 7.24+0.26)4ZM241385 (A 2A , 6.69+0.14)4DPCPX (A 1 , 6.51+0.14)43n-propylxanthine (weak A 2B , 4.30+0.10). This rank order of potency is typical for A 2B -adenosine receptor. 4 Adenosine decreased basal and LPS-stimulated irET production in a concentration-dependent manner. Moreover, NECA but not CGS21680 inhibited LPS-induced irET production. 5 The inhibitory e ect of NECA on LPS-induced irET production was reversed by XAC (pA 2 =8.84+0.12) and DPCPX (pA 2 =8.10+0.22). 6 These results suggested that adenosine increased cyclic AMP formation and inhibited irET production/secretion by guinea-pig tracheal epithelial cells through the activation of a functional adenosine receptor that is most likely the A 2B subtype. This adenosine receptor may be involved in the regulation of the level of ET-1 production/secretion by guinea-pig tracheal epithelial cells in physiological as well as in pathophysiological conditions.

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Activation of Guinea Pig Alveolar Macrophages by Endothelin-1

Cited by 27 publications

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Corresponding distributions of increased endothelin‐B receptor expression and increased endothelin‐1 expression in the aorta of apolipoprotein E‐deficient mice with advanced atherosclerosis

Corresponding distributions of increased endothelin‐B receptor expression and increased endothelin‐1 expression in the aorta of apolipoprotein E‐deficient mice with advanced atherosclerosis

Plasma endothelin concentrations after aneurysmal subarachnoid hemorrhage

Adenosine induces cyclic‐AMP formation and inhibits endothelin‐1 production/secretion in guinea‐pig tracheal epithelial cells through A_2B adenosine receptors

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Activation of Guinea Pig Alveolar Macrophages by Endothelin-1

Cited by 27 publications

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Corresponding distributions of increased endothelin‐B receptor expression and increased endothelin‐1 expression in the aorta of apolipoprotein E‐deficient mice with advanced atherosclerosis

Corresponding distributions of increased endothelin‐B receptor expression and increased endothelin‐1 expression in the aorta of apolipoprotein E‐deficient mice with advanced atherosclerosis

Plasma endothelin concentrations after aneurysmal subarachnoid hemorrhage

Adenosine induces cyclic‐AMP formation and inhibits endothelin‐1 production/secretion in guinea‐pig tracheal epithelial cells through A2B adenosine receptors

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Adenosine induces cyclic‐AMP formation and inhibits endothelin‐1 production/secretion in guinea‐pig tracheal epithelial cells through A_2B adenosine receptors