Specific Binding of Endothelin on Human Bronchial Smooth Muscle Cells in Culture and Secretion of Endothelin-like Material from Bronchial Epithelial Cells

Mattoli, Sabrina; Mezzetti, M; Riva, G; Allegra, L.; Fasoli, A

doi:10.1165/ajrcmb/3.2.145

Cited by 141 publications

(50 citation statements)

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“…Immunoreactivity of endothelin-1 was strongly positive in the (Figure 5d), as previously reported (Ehrenreich et al, 1990;Markewitz et al, 1995;Mattoli et al, 1990). In all the three cases (cases 1, 3 and 8), immunoreactivity was absent in carcinoma cells (Figure 5e).…”

Section: Reduced Expression Of Htr1b and Edn1 In Primary Lung Cancerssupporting

confidence: 86%

Silencing of HTR1B and reduced expression of EDN1 in human lung cancers, revealed by methylation-sensitive representational difference analysis

et al. 2001

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Aberrantly hypermethylated genes in human lung cancers were searched for by a genome scanning technique, methylation-sensitive-representational di erence analysis (MS-RDA). A total of 59 DNA fragments were isolated as those methylated more heavily in either/both of two lung squamous cell carcinoma cell lines, EBC-1 and LK-2, than in a primary culture of normal human bronchial epithelium, NHBE. Thirty-four DNA fragments, whose hypermethylation was con®rmed in primary squamous cell carcinomas, were sequenced. By database searches, 17 of them were shown to be located within 2 kb of putative CpG islands, and ®ve of the 17 DNA fragments had transcribed regions of known genes in their vicinities. By RT ± PCR of the ®ve genes in the carcinoma cell lines and NHBE, decreased expression of HTR1B (5-hydroxytryptamine receptor 1B) and EDN1 (endothelin-1) was observed. Sequencing after bisul®te modi®ca-tion showed that the CpG island in the promoter region of HTR1B was hypermethylated, while that of EDN1 was not. Demethylation and re-expression of HTR1B were observed after treatment of LK-2 cells with 5-aza-2'-deoxycytidine. In primary lung cancers, decreased mRNA expression of HTR1B was observed in 11 of 20 cases, and that of EDN1 was in 16 of 20 cases. Immunohistochemical analysis of endothelin-1 con®rmed that its immunoreactivity was reduced in squamous cell carcinoma cells compared with that in normal bronchial epithelial cells. Considering that endothelin-1 induces apoptosis in melanoma cells and that silencing of endothelin receptor B is observed in prostate cancers, its reduced expression was speculated to confer a growth advantage to lung cancer cells. MS-RDA was shown to isolate DNA fragments that are hypermethylated and silenced, such as HTR1B, and those whose expressions are altered and the methylation statuses outside the promoter region are altered, such as EDN1. Oncogene (2001) 20, 7505 ± 7513.

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Section: Reduced Expression Of Htr1b and Edn1 In Primary Lung Cancerssupporting

confidence: 86%

Silencing of HTR1B and reduced expression of EDN1 in human lung cancers, revealed by methylation-sensitive representational difference analysis

et al. 2001

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“…By use of ['251]-ET-l, specific binding sites of high density were detected in smooth muscle of human isolated trachea and bronchus (Henry et al, 1990;McKay et al, 1991), in human cultured bronchial smooth muscle cells (Mattoli et al, 1990) and in human lung membranes (Brink et al, 1991). The ET-1 EC-% in human bronchus is generally in the 10-30 nM range (Henry et al, 1990; Hemsen et al, 1990;Advenier et al, 1990;Brink et al, 1991;McKay et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

“…This observation has been confirmed (Hay, 1989;Maggi et al, 1989;Henry et al, 1990) and extended to isolated airway tissues from a variety of species including rat (Turner et al, 1989), ferret (Lee et al, 1990), rabbit (Grunstein et al, 1991) and man (Henry et al, 1990; Hemsen et al, 1990;Advenier et al, 1990;Brink et al, 1991;McKay et al, 1991). In fact, it has been proposed that the endothelins play a role in the pathophysiology of pulmonary disorders including asthma and pulmonary hypertension (Cernacek & Stewart, 1989;Mattoli et al, 1991a;Springall et al, 1991;.By use of ['251]-ET-l, specific binding sites of high density were detected in smooth muscle of human isolated trachea and bronchus (Henry et al, 1990;McKay et al, 1991), in human cultured bronchial smooth muscle cells (Mattoli et al, 1990) and in human lung membranes (Brink et al, 1991). The ET-1 EC-% in human bronchus is generally in the 10-30 nM range (Henry et al, 1990; Hemsen et al, 1990;Advenier et al, 1990;Brink et al, 1991;McKay et al, 1991).…”

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confidence: 99%

Endothelin‐induced contraction and mediator release in human bronchus

Hay

Hubbard

Undem

1993

British J Pharmacology

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1 To elucidate the role of acetylcholine and various autacoids in endothelin-I (ET-l)-induced contraction in human bronchus, the effects of various receptor antagonists were examined. In addition, the ability of ET-1 to stimulate the release of histamine, peptidoleukotrienes and prostanoids was determined. 2 ET-1 was a potent and effective contractile agonist in human bronchus, possessing similar potency and efficacy to leukotriene D4 (LTD4); EC50 (-log M): ET-1 = 7.76 ± 0.09, n = 7; LTD4 = 8.46 ± 0.53, n = 7; P>0.2; maximum response (% 10PiM pre-carbachol): ET-1 = 103.8 ± 17.4, n = 7; LTD4=95.5±9.3, n=7; P>0.6.3 The cyclo-oxygenase inhibitor, sodium meclofenamate (1 pM) or the potent and selective thromboxane receptor antagonist, SQ 29,548 (1 pLM) were without significant effect on ET-1 concentrationresponse curves. 4 In the presence of sodium meclofenamate (1 I1M), the muscarinic receptor antagonist, atropine(1 fLM), the platelet activating factor (PAF) receptor antagonist, WEB 2086 (1 jiM) or the combination of the Hi-histamine receptor antagonist, mepyramine (10#iM) and the leukotriene receptor antagonist, SK&F 104353 (10 pM), were without marked effect on ET-1 concentration-response curves. In addition, the combination of all four receptor antagonists did not antagonize ET-1-induced contraction.5 ET-1 (0.3 pM) did not stimulate the release of histamine or immunoreactive leukotrienes from human bronchus.6 ET-1 (0.3 f4M) significantly stimulated the release of prostaglandin D2 (PGD2), 9a, 11p PGF2 (PGD2 metabolite), PGE2, 6-keto PGF1, (PGI2 metabolite), PGF2,, and thromboxane B2 (TxB2) a lower concentration, 10 nM, was without effect on prostanoid release. The production of PGD2 was increased 7.5 fold, whereas the release of the other prostanoids was stimulated only about 1.6 to 2.7 fold. 7 These data provide evidence that ET-1 elicits contraction of human isolated bronchus predominantly via a direct mechanism with no significant involvement of the release of acetylcholine, leukotrienes, histamine or PAF. Although IntroductionYanagisawa and co-workers described the isolation, purification, cloning and pharmacological characterization of a potent vasoconstrictor peptide, designated endothelin, which was released from porcine aortic endothelial cells (Yanagisawa et al., 1988). Endothelin is a 21-amino acid peptide, with two sets of intrachain disulphide bridges, which bears a close structural homology with the sarafotoxins, a group of snake venom toxins (Lee & Chiappinelli, 1988;Kloog et al., 1988). Subsequent research indicated that endothelin, named endothelin-1 (ET-1), is only one member of a family of mammalian endothelins; Thus, Inoue and co-workers cloned three distinct ET-related genes by screening a human genomic DNA library (Inoue et al., 1989). These three 21-amino acid peptides, which have only minor differences in amino acid sequence, were designated ET-1 (the orginal porcine/human ET), ET-2 (two amino acid substitution from ET-1) and ET-3 (six amino acid substitution from ET-1) (Yanagisawa & Ma...

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“…The endothelins are a family of 21-amino acid peptides that are the most potent vasoconstrictor substances yet described (9). ET-1 is the dominant form in the lung and is expressed by multiple cell types, principally vascular endothelium and bronchial epithelium (10,11). Both ET A and ET B receptors mediate the effects of ET-1.…”

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Endothelin-1 and O2-Mediated Pulmonary Hypertension in Neonatal Rats: A Role for Products of Lipid Peroxidation

et al. 2000

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We hypothesized that reactive O 2 species, or their intermediary products, generated during exposure to elevated O 2 lead to pathologic endothelin-1 expression in the newborn lung. Endothelin-1 expression and 8-isoprostane content (an in vivo marker of lipid peroxidation) were examined and found to be elevated (p Ͻ 0.05) in the lungs of newborn rats with abnormal lung morphology and pulmonary hypertension, as assessed by right ventricular hypertrophy, after a 14-d exposure to 60% O 2 . The antioxidant and lipid hydroperoxide scavenger, U74389G (10 mg/kg), given by daily i.p. injection prevented O 2 -dependent right ventricular hypertrophy (p Ͻ 0.05 compared with vehicletreated controls), but had no effect on abnormal lung morphology. Additionally, we observed that 8-isoprostane caused marked endothelin-1 mRNA up-regulation in vitro in primary rat fetal lung cell cultures. We conclude that reactive O 2 species, or their bioactive intermediaries, are causative in O 2 -mediated pulmonary hypertension and endothelin-1 up-regulation. It is likely that the bioactive lipid peroxidation product, 8-isoprostane, plays a key role in pathologic endothelin-1 expression and pulmonary hypertension during oxidant stress. The use of sustained supplemental O 2 and mechanical ventilation in premature infants with respiratory failure is associated with the development of bronchopulmonary dysplasia (BPD), a chronic neonatal lung injury (1). Characteristic features of BPD include a dysregulation of lung growth, including fibroproliferative changes (2). This condition remains an important cause of mortality and morbidity during early infancy and in later childhood (3). There are currently no rational or effective therapies available for the prevention or treatment of BPD and its accompanying complications. The putative central role for O 2 toxicity in the pathogenesis of BPD has led to considerable interest in the use of antioxidant therapies as preventive and therapeutic agents (4).Pulmonary hypertension is a common complication in infants with established BPD (5) and early respiratory failure (6), and is an important adverse factor in their outcome (7). An increased expression of ET-1 is observed in adult patients with pulmonary hypertension (8), which may play a causative role. The endothelins are a family of 21-amino acid peptides that are the most potent vasoconstrictor substances yet described (9). ET-1 is the dominant form in the lung and is expressed by multiple cell types, principally vascular endothelium and bronchial epithelium (10, 11). Both ET A and ET B receptors mediate the effects of ET-1. These receptors are both expressed in vascular and bronchial smooth muscle cells (11, 12), whereas vascular endothelial cells express only ET B receptors (13).Factors known to up-regulate ET-1 include hypoxia (14, 15), proinflammatory cytokines (16), and shear stress (17). We have recently described a newborn rat model with BPD-like histopathology (18)

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Specific Binding of Endothelin on Human Bronchial Smooth Muscle Cells in Culture and Secretion of Endothelin-like Material from Bronchial Epithelial Cells

Cited by 141 publications

References 17 publications

Silencing of HTR1B and reduced expression of EDN1 in human lung cancers, revealed by methylation-sensitive representational difference analysis

Silencing of HTR1B and reduced expression of EDN1 in human lung cancers, revealed by methylation-sensitive representational difference analysis

Endothelin‐induced contraction and mediator release in human bronchus

Endothelin-1 and O2-Mediated Pulmonary Hypertension in Neonatal Rats: A Role for Products of Lipid Peroxidation

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