PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20186146-6 2010 The effects of ET1 and aldosterone were blocked by bosentan, an ET type-A/B receptor (ETA/BR) antagonist, and eplerenone, a selective mineralocorticoid receptor (MR) blocker, respectively. Bosentan 51-59 endothelin 1 Homo sapiens 15-18 21777087-6 2011 Bosentan (10(-5) mol/L), an inhibitor of endothelin-1 (ET-1) receptors, corrected the attenuated vasodilatation observed with r-HuEPO and inhibited the vasoconstriction induced by flow in the presence of r-HuEPO and L-NAME. Bosentan 0-8 endothelin 1 Homo sapiens 41-53 21777087-6 2011 Bosentan (10(-5) mol/L), an inhibitor of endothelin-1 (ET-1) receptors, corrected the attenuated vasodilatation observed with r-HuEPO and inhibited the vasoconstriction induced by flow in the presence of r-HuEPO and L-NAME. Bosentan 0-8 endothelin 1 Homo sapiens 55-59 20625315-4 2010 Endothelin-1 treatment led to a time- and concentration-dependent increase in cytosolic phosphoSmad2C, which was inhibited by the mixed endothelin receptor antagonist bosentan and the T[beta]RI antagonist SB431542. Bosentan 167-175 endothelin 1 Homo sapiens 0-12 20625315-6 2010 Endothelin-1-stimulated proteoglycan synthesis was partially inhibited (40%) by SB431542 and completely blocked by bosentan. Bosentan 115-123 endothelin 1 Homo sapiens 0-12 20131241-11 2010 ET-1 receptor antagonists, such as bosentan, may represent a useful therapeutic tool in the treatment of excessive scarring and fibrosis-related diseases. Bosentan 35-43 endothelin 1 Homo sapiens 0-4 19967386-4 2010 The discovery of two receptor subtypes in 1990, ET(A) and ET(B), permitted optimization of the first dual ET-1 receptor antagonist in 1993 by Dr. Clozel"s team, who entered clinical development with bosentan, which was offered to patients with pulmonary arterial hypertension in 2001. Bosentan 199-207 endothelin 1 Homo sapiens 106-110 19747014-1 2009 Bosentan (Tracleer) is an orally administered dual endothelin-1 (ET-1) receptor antagonist approved in the EU for reducing the number of new digital ulcers in patients with systemic sclerosis and ongoing digital ulcer disease. Bosentan 0-8 endothelin 1 Homo sapiens 51-63 19660388-5 2010 The primary objective of this study was to determine whether the dual endothelin-1 antagonist bosentan improves pulmonary hemodynamics and functional capacity in patients with proximal chronic thromboembolic pulmonary hypertension waiting for pulmonary endarterectomy. Bosentan 94-102 endothelin 1 Homo sapiens 70-82 20034342-1 2010 Bosentan is a dual endothelin-1 (ET-1) receptor antagonist that has affinity for ET-1 receptors A and B. Bosentan 0-8 endothelin 1 Homo sapiens 19-31 19850966-4 2009 To elucidate the anti-inflammatory properties of the dual endothelin receptor antagonist bosentan that targets both endothelin receptor subtypes A (ET(A)R) and B (ET(B)R), its effect on the TNFalpha/ET-1/GM-CSF network was investigated. Bosentan 89-97 endothelin 1 Homo sapiens 199-203 19850966-9 2009 ET-1- and TNFalpha-induced GM-CSF expression were both reduced by bosentan as well as by specific inhibition of either ET(A)R, ET(B)R, p38(MAPK) or ERK-1/-2. Bosentan 66-74 endothelin 1 Homo sapiens 0-4 19850966-11 2009 Since bosentan impairs ET-1 autoregulation and TNFalpha-induced ET-1 release, as well as TNFalpha- and ET-1-induced GM-CSF release, the present data suggest therapeutic utility for bosentan in treating particularly the early stages of chronic inflammatory airway diseases. Bosentan 6-14 endothelin 1 Homo sapiens 23-27 19850966-11 2009 Since bosentan impairs ET-1 autoregulation and TNFalpha-induced ET-1 release, as well as TNFalpha- and ET-1-induced GM-CSF release, the present data suggest therapeutic utility for bosentan in treating particularly the early stages of chronic inflammatory airway diseases. Bosentan 6-14 endothelin 1 Homo sapiens 64-68 19850966-11 2009 Since bosentan impairs ET-1 autoregulation and TNFalpha-induced ET-1 release, as well as TNFalpha- and ET-1-induced GM-CSF release, the present data suggest therapeutic utility for bosentan in treating particularly the early stages of chronic inflammatory airway diseases. Bosentan 6-14 endothelin 1 Homo sapiens 64-68 18951296-2 2008 Endothelin-1 may underlie the pathogenesis of lung fibrosis, therefore it was hypothesized that the oral dual endothelin receptor antagonist bosentan may have efficacy for the treatment of IPF. Bosentan 141-149 endothelin 1 Homo sapiens 0-12 19217622-7 2009 Endothelin-1 stimulated an increase in the 6:4 position sulfation ratio on the disaccharides of the GAG chains, an effect that was blocked by bosentan. Bosentan 142-150 endothelin 1 Homo sapiens 0-12 19417139-9 2009 Inhibition of the ET-1 receptor ETR-A with bosentan restored the antiproliferative effects of PEP005 in Colo205-R cells and decreased the invasive properties of this cell line. Bosentan 43-51 endothelin 1 Homo sapiens 18-22 19791841-1 2009 Bosentan (Tracleer) is an orally administered dual endothelin-1 (ET-1) receptor antagonist approved for use in patients with WHO class II (mildly symptomatic) pulmonary arterial hypertension (PAH). Bosentan 0-8 endothelin 1 Homo sapiens 51-63 18470553-2 2008 Endothelin (ET)-1 is elevated in SCD and appears to play a key role in many of the pathologic processes in this disease, including PH, suggesting that endothelin receptor antagonists such as bosentan may be effective in treating patients with SCD, particularly those with PH. Bosentan 191-199 endothelin 1 Homo sapiens 0-17 18694375-3 2008 OBJECTIVE: To evaluate the role of the endothelin-1 (ET-1) pathway in IPF pathogenesis and the effects of therapeutic targeting with bosentan, an ET-1 antagonist. Bosentan 133-141 endothelin 1 Homo sapiens 146-150 17767746-4 2007 Although a relationship between raised levels of ET-1 and clinical phenotype is yet to be identified, early evidence from studies of ET-1 blockade with drugs such as bosentan is encouraging. Bosentan 166-174 endothelin 1 Homo sapiens 133-137 17663518-3 2007 Bosentan, a dual ET (A/B)-receptor antagonist, was used to inhibit the binding of endothelin-1 and its receptors and cut down its biological role. Bosentan 0-8 endothelin 1 Homo sapiens 82-94 18243424-7 2008 Two ET-1 receptor antagonists, orally active, can be used: bosentan (ET(A)/ET(B)=20) is nonselective and sitaxentan (ET(A)/ET(B)=6500) is highly selective. Bosentan 59-67 endothelin 1 Homo sapiens 4-8 18295521-3 2008 The objective of this study was to further elucidate the pro-inflammatory effects of ET-1 on ETB receptors in cultured human monocytes (10(5)/20 h) compared with non-specific stimulation with LPS in vitro and to define the antagonizing effects of bosentan, a dual ETA/ETB-receptor antagonist, on inflammatory mediator production. Bosentan 247-255 endothelin 1 Homo sapiens 85-89 17322637-0 2007 Effect of bosentan on plasma endothelin-1 concentration in patients with pulmonary arterial hypertension. Bosentan 10-18 endothelin 1 Homo sapiens 29-41 16614599-1 2006 OBJECTIVES: To describe the effect of bosentan and its dual inhibition of endothelin-1 ETA and ETB receptors on digital ulcers in patients with systemic sclerosis (SSc). Bosentan 38-46 endothelin 1 Homo sapiens 74-86 16820593-15 2006 ET-1 antagonism with bosentan stimulates translocation of PKClambda and leads to increased PKC activity and NO production. Bosentan 21-29 endothelin 1 Homo sapiens 0-4 16866076-3 2006 The endothelin-1 receptor antagonist bosentan inhibits the action of endothelin-1 at both receptor subtypes (ET(A) and ET(B) receptors) and has been approved for PAH therapy since 2001. Bosentan 37-45 endothelin 1 Homo sapiens 4-16 15317671-4 2004 Bosentan (20-50 microM) significantly inhibited endothelin-1- or platelet-derived growth factor (PDGF)-mediated PASMC growth and [3H]thymidine uptake. Bosentan 0-8 endothelin 1 Homo sapiens 48-60 16248783-5 2005 However, to date the only prescribed ET-1 antagonist is bosentan for pulmonary arterial hypertension. Bosentan 56-64 endothelin 1 Homo sapiens 37-41 16248783-6 2005 Bosentan is a "dual" ET-1 antagonist (i.e. it acts on both ET(A) and ET(B) receptors). Bosentan 0-8 endothelin 1 Homo sapiens 21-25 15610070-11 2005 The vaso-constrictor response induced by intra-arterial infusion of ET-1 was attenuated significantly by bosentan (P<0.001). Bosentan 105-113 endothelin 1 Homo sapiens 68-72 15811199-6 2005 Recently, a dual inhibitor of endothelin-1, bosentan, has been successfully evaluated in clinical trials in PAH patients. Bosentan 44-52 endothelin 1 Homo sapiens 30-42 15633133-2 2005 Endothelin-1, a potent vasoconstrictor, is likely to play a role in the pathogenesis of primary pulmonary hypertension, and, in 2 recent trials, the dual endothelin receptor antagonist bosentan has shown beneficial effects in this disease. Bosentan 185-193 endothelin 1 Homo sapiens 0-12 15568889-22 2004 In healthy subjects, bosentan doses >300 mg increase plasma levels of endothelin-1. Bosentan 21-29 endothelin 1 Homo sapiens 73-85 15246919-1 2004 Bosentan, an endothelin-1 antagonist that can be administered orally, has been shown to be effective in the treatment of idiopathic pulmonary arterial hypertension and may be of benefit to patients with the Eisenmenger syndrome. Bosentan 0-8 endothelin 1 Homo sapiens 13-25 15063187-9 2004 Furthermore, bosentan, a pharmacological inhibitor of Endothelin-1 signaling caused a loss of I56i-lacZ expression in the most distal aspects of the expression domain, corresponding to the area of Dlx-6 expression previously shown to be under the control of Endothelin-1. Bosentan 13-21 endothelin 1 Homo sapiens 54-66 15063187-9 2004 Furthermore, bosentan, a pharmacological inhibitor of Endothelin-1 signaling caused a loss of I56i-lacZ expression in the most distal aspects of the expression domain, corresponding to the area of Dlx-6 expression previously shown to be under the control of Endothelin-1. Bosentan 13-21 endothelin 1 Homo sapiens 258-270 14736539-9 2004 Bosentan, an orally active, dual ET-1 receptor antagonist has been shown to improve symptoms, exercise capacity, hemodynamics, echocardiographic parameters and the outcome of patients with severe PAH, and it has been approved for clinical use in many countries. Bosentan 0-8 endothelin 1 Homo sapiens 33-37 12063458-4 2002 Therefore we studied the effects of endothelin receptor blockers (BQ-123 and bosentan) on hyperglycemia-induced endothelin-1 production and cellular injury after ischemia-reperfusion. Bosentan 77-85 endothelin 1 Homo sapiens 112-124 15658881-9 2004 The US FDA has approved a number of novel treatments, including long-acting oral ET-1 receptor antagonists such as bosentan and short-acting parenteral prostacyclin analogs, such as epoprostenol, for PAH. Bosentan 115-123 endothelin 1 Homo sapiens 81-85 14506620-3 2003 The goal of the present studies was to determine if ET-1 is involved in upregulating the expression of AVP V2 mRNA in the IMCD of CM by using a mixed ETA/ETB receptor antagonist bosentan. Bosentan 178-186 endothelin 1 Homo sapiens 52-56 14506620-10 2003 This study demonstrated that AVP V2 and AQP2 mRNA are upregulated in CM hamsters and these upregulations are attenuated by bosentan treatment, suggesting that ET-1 plays a role in upregulating the expression of AVP V2 mRNA in CM hamsters. Bosentan 123-131 endothelin 1 Homo sapiens 159-163 12686474-9 2003 On the other hand, bosentan and BQ788 caused a reduction in the numbers of endothelin-1-secreting cells. Bosentan 19-27 endothelin 1 Homo sapiens 75-87 12686474-11 2003 The receptor antagonists, bosentan and BQ788, inhibited basal secretion of endothelin-1. Bosentan 26-34 endothelin 1 Homo sapiens 75-87 12628956-10 2003 CONCLUSIONS: Experimental overcirculation-induced pulmonary arterial hypertension appears to be causally related to an activation of the pulmonary ET-1 system and as such is completely prevented by the dual endothelin receptor antagonist bosentan. Bosentan 238-246 endothelin 1 Homo sapiens 147-151 12547713-6 2003 Co-treatment with Bosentan abolished the actions of ET-1. Bosentan 18-26 endothelin 1 Homo sapiens 52-56 11973408-6 2002 Bosentan (10 microM, dual ETA/B receptor antagonist) reduced (p < 0.05) immunoreactive ET-1 content in control cells. Bosentan 0-8 endothelin 1 Homo sapiens 90-94 11973408-7 2002 Bosentan prevented exogenous ET-1-induced endothelial cell ET-1 loading, suggesting that exogenous ET-1 is partly recycled. Bosentan 0-8 endothelin 1 Homo sapiens 29-33 11973408-7 2002 Bosentan prevented exogenous ET-1-induced endothelial cell ET-1 loading, suggesting that exogenous ET-1 is partly recycled. Bosentan 0-8 endothelin 1 Homo sapiens 59-63 11973408-7 2002 Bosentan prevented exogenous ET-1-induced endothelial cell ET-1 loading, suggesting that exogenous ET-1 is partly recycled. Bosentan 0-8 endothelin 1 Homo sapiens 59-63 11973408-8 2002 PreproET-1 mRNA levels were reduced (p < 0.05) by exogenous ET-1 after 24 h, an effect blocked by BQ788 and bosentan. Bosentan 111-119 endothelin 1 Homo sapiens 6-10 14727963-2 2002 Orally administered bosentan effectively prevents endothelin 1-induced vasoconstriction in pulmonary vessels in patients with pulmonary arterial hypertension. Bosentan 20-28 endothelin 1 Homo sapiens 50-62 11447300-12 2001 Furthermore, the contribution of ET-1 to human hypertension appears more convincing since bosentan was shown to decrease blood pressure in hypertensive subjects. Bosentan 90-98 endothelin 1 Homo sapiens 33-37 11515898-8 2001 Bosentan reduced the hypoxia and reoxygenation-induced elevation of ET-1 and iNOS mRNA at the end of recovery (p < 0.05). Bosentan 0-8 endothelin 1 Homo sapiens 68-72 10233186-5 1999 AIM: To investigate whether acute gastroduodenal injury induced in humans by aspirin can be prevented by the endothelin-1 antagonist, bosentan. Bosentan 134-142 endothelin 1 Homo sapiens 109-121 11407110-6 2001 Vasopeptidase inhibitor, such as omapatrilat, and endothelin-1 antagonist, such as bosentan, may become future agents approved for the reduction of morbidity and mortality with hypertension. Bosentan 83-91 endothelin 1 Homo sapiens 50-62 11238005-6 2001 Treatment of the animals with the ET receptor antagonist bosentan resulted in a substantial decrease in the concentrations of tumor necrosis factor-alpha, IL-4, IL-1beta, interferon-gamma, and ET-1 in bronchoalveolar lavage fluid. Bosentan 57-65 endothelin 1 Homo sapiens 193-197 11187978-7 2000 Bosentan, the non-selective ET(A)/ET(B) antagonist, when given by dialysis at the site of injection, reduced the area of both the ET-1-induced pallor and surrounding flare by 41 and 26%, respectively. Bosentan 0-8 endothelin 1 Homo sapiens 130-134 10433505-10 1999 These actions of ET-1 were almost completely prevented by the ET(A) receptor antagonist FR 139317 (1 microM) and the ET(A)/ET(B) receptor antagonist bosentan (10 microM), whereas the ET(B) receptor antagonist BQ 788 (1 microM) had no effect. Bosentan 149-157 endothelin 1 Homo sapiens 17-21 10908213-2 2000 This trial was designed to assess the hemodynamic effects of bosentan, an endothelin receptor antagonist, in patients with PHT, in which local overproduction of endothelin-1 (ET-1) is thought to play a pathogenic role. Bosentan 61-69 endothelin 1 Homo sapiens 161-173 10908213-2 2000 This trial was designed to assess the hemodynamic effects of bosentan, an endothelin receptor antagonist, in patients with PHT, in which local overproduction of endothelin-1 (ET-1) is thought to play a pathogenic role. Bosentan 61-69 endothelin 1 Homo sapiens 175-179 10585047-4 1999 This study was carried out using an established model of hypoxia and reoxygenation to determine whether endothelin-1 blockade with Bosentan could prevent hypoxia-reoxygenation-induced pulmonary hypertension and reoxygenation injury. Bosentan 131-139 endothelin 1 Homo sapiens 104-116 9777021-5 1998 Contractions induced by endothelin-1 were antagonized by FR 139,317 and bosentan, but not by BQ 788. Bosentan 72-80 endothelin 1 Homo sapiens 24-36 9826312-12 1998 Plasma ET-1 levels increased after bosentan, but baseline levels of the other hormones were unchanged. Bosentan 35-43 endothelin 1 Homo sapiens 7-11 9635152-3 1998 The vasodilator and vasoconstrictor components of the biphasic responses to endothelin-1 and sarafotoxin 6c were reduced by bosentan, and the endothelin receptor antagonist reduced baseline systemic arterial and hind-limb perfusion pressures. Bosentan 124-132 endothelin 1 Homo sapiens 76-88 9635152-6 1998 The results of the present study show that bosentan attenuates vasodilator and vasoconstrictor responses to endothelin-1 and sarafotoxin 6c and vasoconstrictor responses to lower doses of angiotensin II in the hind-limb vascular bed of the cat. Bosentan 43-51 endothelin 1 Homo sapiens 108-120 9145775-3 1997 Bosentan and FR 139317 (each 10 microM) produced a small shift in response curves to endothelin-1 (1.6- and 1.5-fold, respectively). Bosentan 0-8 endothelin 1 Homo sapiens 85-97 9176269-6 1997 The combined ETA-ETB antagonist, bosentan, also inhibited ET-1-induced mitogenesis (IC50 = 20 nM, slope of 0.60). Bosentan 33-41 endothelin 1 Homo sapiens 58-62 8035319-6 1994 In vivo, bosentan inhibited the pressor response to big ET-1 both after i.v. Bosentan 9-17 endothelin 1 Homo sapiens 56-60 8823230-8 1996 Plasma ET-1 increased maximally twofold (oral) and threefold (intravenous), and this increase was directly related to bosentan plasma concentrations according to an Emax model. Bosentan 118-126 endothelin 1 Homo sapiens 7-11 8823230-9 1996 Bosentan reversed the vasoconstrictor effect of ET-1 measured in the skin microcirculation. Bosentan 0-8 endothelin 1 Homo sapiens 48-52 8823230-13 1996 CONCLUSION: Bosentan is an orally bioavailable, well-tolerated, and active ET-1 antagonist with a low clearance and a moderate volume of distribution. Bosentan 12-20 endothelin 1 Homo sapiens 75-79 8751489-10 1996 Furthermore, contractions evoked by endothelin-1 in the left anterior descending coronary and pulmonary arteries were antagonized by the combined endothelinA- and endothelinB-receptor blocker bosentan. Bosentan 192-200 endothelin 1 Homo sapiens 36-48 7663155-4 1995 This was confirmed by experiments in which the binding activity of endothelin-1 to various chimeric endothelin receptors was monitored in the presence and absence of competitive endothelin receptor antagonists such as BQ-123 and bosentan. Bosentan 229-237 endothelin 1 Homo sapiens 67-79 7663155-4 1995 This was confirmed by experiments in which the binding activity of endothelin-1 to various chimeric endothelin receptors was monitored in the presence and absence of competitive endothelin receptor antagonists such as BQ-123 and bosentan. Bosentan 229-237 endothelin 1 Homo sapiens 67-77 9069452-5 1997 The mitogenic effect of endothelial cells in coculture resulted from ET-1 production since it was suppressed by bosentan, a mixed specific ET-1 receptor antagonist. Bosentan 112-120 endothelin 1 Homo sapiens 69-73 9069452-5 1997 The mitogenic effect of endothelial cells in coculture resulted from ET-1 production since it was suppressed by bosentan, a mixed specific ET-1 receptor antagonist. Bosentan 112-120 endothelin 1 Homo sapiens 139-143 9265559-6 1997 The dose-dependent systemic vasoconstriction evoked by ET-1 infusion was reduced after administration of the combined ETA and ETB receptor antagonist bosentan as well as the selective ETA receptor blockers BMS-182874 and TBC-11251 indicating that this effect is primarily mediated by ETA receptors. Bosentan 150-158 endothelin 1 Homo sapiens 55-59 9265559-12 1997 The plasma levels of ET-1 increased following the non-selective ET receptor antagonist bosentan but were unaffected by selective ETA receptor antagonism. Bosentan 87-95 endothelin 1 Homo sapiens 21-25 9265559-24 1997 The concentration-dependent contraction evoked by ET-1 in human vessels in vitro (LAD, IMA, PA, SV) was reduced after incubation with BQ-123 and bosentan. Bosentan 145-153 endothelin 1 Homo sapiens 50-54 8940346-12 1996 Endothelin-1, a vasoconstrictor peptide that is known to promote fibroblast-embedded collagen gel contraction, appeared to be partially involved in the IGF-I- and IGFBP-1-induced gel contraction, because the addition of an endothelin receptor antagonist (Bosentan or BE-18257B at 1 microg/ml) moderately suppressed the IGF-I- and IGFBP-1-induced gel contraction (P < 0.01). Bosentan 255-263 endothelin 1 Homo sapiens 0-12 7658874-2 1995 The role of endogenously released endothelin-1 in the maintenance of vascular tone in chronic heart failure was assessed by acute administration of an endothelin receptor antagonist, bosentan. Bosentan 183-191 endothelin 1 Homo sapiens 34-46 7658874-8 1995 Plasma endothelin-1 concentrations rose more than twofold from baseline in bosentan recipients while big-endothelin-1 concentrations were unchanged. Bosentan 75-83 endothelin 1 Homo sapiens 7-19 8587420-1 1995 The binding characteristics and localization of bosentan, an orally active endothelin-1 (ET-1) antagonist, were studied on sections of human coronary artery by in vitro autoradiography. Bosentan 48-56 endothelin 1 Homo sapiens 75-87 8587420-1 1995 The binding characteristics and localization of bosentan, an orally active endothelin-1 (ET-1) antagonist, were studied on sections of human coronary artery by in vitro autoradiography. Bosentan 48-56 endothelin 1 Homo sapiens 89-93 8587420-2 1995 Competition studies were performed to determine the ability of bosentan to prevent [125I]ET-1 binding to the coronary vasculature. Bosentan 63-71 endothelin 1 Homo sapiens 89-93 8587420-3 1995 The effects of bosentan on ET-1-induced contraction of the coronary artery were also studied in vitro. Bosentan 15-23 endothelin 1 Homo sapiens 27-31 8587420-5 1995 Unlabeled bosentan prevented [125I]ET-1 binding to this vessel in a concentration-dependent manner, and functional studies indicated that bosentan antagonizes ET-1--induced constriction. Bosentan 10-18 endothelin 1 Homo sapiens 35-39 8587420-5 1995 Unlabeled bosentan prevented [125I]ET-1 binding to this vessel in a concentration-dependent manner, and functional studies indicated that bosentan antagonizes ET-1--induced constriction. Bosentan 138-146 endothelin 1 Homo sapiens 159-163 8587420-6 1995 These data show that bosentan is able to reduce ET-1 binding to the human coronary artery and ET-1 constrictor effects in vitro. Bosentan 21-29 endothelin 1 Homo sapiens 48-52 8587420-6 1995 These data show that bosentan is able to reduce ET-1 binding to the human coronary artery and ET-1 constrictor effects in vitro. Bosentan 21-29 endothelin 1 Homo sapiens 94-98 8587420-7 1995 Bosentan is an orally active ET-1 antagonist, and these results suggest that this compound might be used to block the effects of locally released ET-1 in pathologic conditions, such as atherosclerosis, angina, and myocardial ischemia. Bosentan 0-8 endothelin 1 Homo sapiens 29-33 8587420-7 1995 Bosentan is an orally active ET-1 antagonist, and these results suggest that this compound might be used to block the effects of locally released ET-1 in pathologic conditions, such as atherosclerosis, angina, and myocardial ischemia. Bosentan 0-8 endothelin 1 Homo sapiens 146-150 34982346-9 2022 ET-1 mediated mRNA expression of GAG synthesizing enzymes C4ST-1 and ChSy-1 was also blocked by TGBFR1 antagonists, SB431542, broad spectrum ET receptor antagonist bosentan, DPI and ROS scavenger N-acetyl-L-cysteine. Bosentan 164-172 endothelin 1 Homo sapiens 0-4 34837677-5 2021 Results: ET-1 (100 nM) and EGF (100 ng/ml) stimulated ERK1/2 phosphorylation and inhibited in the presence of bosentan (ET receptor inhibitor), AG1478 (EGFR inhibitor), and DPI (NOX antagonist). Bosentan 110-118 endothelin 1 Homo sapiens 9-13 34837677-6 2021 Also, ET-1 treatment increased CHSY1 enzyme level; this response was suppressed by bosentan, AG1478, DPI, and SB431542, TGF-beta receptor antagonist. Bosentan 83-91 endothelin 1 Homo sapiens 6-10 34199777-5 2021 Carbon monoxide (CO) activated the ECE-1/endothelin-1 (ET-1) pathway, which could account for the protumoral effects of HO-1 in p53 wild-type cells, as demonstrated after treatment with bosentan (an antagonist of both ETRA and ETRB endothelin-1 receptors). Bosentan 186-194 endothelin 1 Homo sapiens 41-53 34199777-5 2021 Carbon monoxide (CO) activated the ECE-1/endothelin-1 (ET-1) pathway, which could account for the protumoral effects of HO-1 in p53 wild-type cells, as demonstrated after treatment with bosentan (an antagonist of both ETRA and ETRB endothelin-1 receptors). Bosentan 186-194 endothelin 1 Homo sapiens 55-59 34199777-5 2021 Carbon monoxide (CO) activated the ECE-1/endothelin-1 (ET-1) pathway, which could account for the protumoral effects of HO-1 in p53 wild-type cells, as demonstrated after treatment with bosentan (an antagonist of both ETRA and ETRB endothelin-1 receptors). Bosentan 186-194 endothelin 1 Homo sapiens 232-244 34199777-6 2021 Surprisingly, in cells with a non-active p53 or a mutated p53 with gain-of-function, ECE-1-produced ET-1 acted as a protective molecule, since treatment with bosentan led to increased efficiency for spheres formation and percentage of cancer stem cells (CSCs) markers. Bosentan 158-166 endothelin 1 Homo sapiens 100-104 35527471-5 2022 The TGF-beta receptor antagonist, SB431542 and the mixed ETA and ETB receptor antagonist bosentan, inhibited ET-1-mediated phospho-Smad2L level. Bosentan 89-97 endothelin 1 Homo sapiens 109-113 35373585-7 2022 RESULTS: Treatment with bosentan increased plasma ET-1 in both OB and HW groups. Bosentan 24-32 endothelin 1 Homo sapiens 50-54 35373585-10 2022 Overall, absolute plasma concentrations of ET-1 following treatment with bosentan were significantly associated with kcal/day of fat (r=0.488, p=0.005), percentage of fat utilization (r=0.415, p=0.020), and inversely associated with the percentage of carbohydrates (r=-0.419, p=0.019), and respiratory exchange ratio (r=-0.407, p=0.023). Bosentan 73-81 endothelin 1 Homo sapiens 43-47 33359621-7 2021 Bosentan (1E-7 M) and macitentan (1E-8 M, 3E-8 M, 1E-7 M) inhibited ET-1 induced contractions, whereas vardenafil (1E-6 M, 3E-6 M, 1E-5 M) inhibited only the NE induced part of the contractions. Bosentan 0-8 endothelin 1 Homo sapiens 68-72 33856498-2 2021 Bosentan (BST) is the first approved oral targeted drug of endothelin-1 (ET-1) receptor antagonists for the treatment of PAH. Bosentan 0-8 endothelin 1 Homo sapiens 73-77 33856498-2 2021 Bosentan (BST) is the first approved oral targeted drug of endothelin-1 (ET-1) receptor antagonists for the treatment of PAH. Bosentan 10-13 endothelin 1 Homo sapiens 59-71 33856498-2 2021 Bosentan (BST) is the first approved oral targeted drug of endothelin-1 (ET-1) receptor antagonists for the treatment of PAH. Bosentan 10-13 endothelin 1 Homo sapiens 73-77 33856498-0 2021 The Influence of Bosentan on MicroRNA-27a/PPARgamma/ET-1 Signaling Pathway in Pulmonary Artery Hypertension. Bosentan 17-25 endothelin 1 Homo sapiens 52-56 33856498-2 2021 Bosentan (BST) is the first approved oral targeted drug of endothelin-1 (ET-1) receptor antagonists for the treatment of PAH. Bosentan 0-8 endothelin 1 Homo sapiens 59-71 32765401-4 2020 A preliminary study in patients with MS showed that CBF could be restored to normal values after a single dose of 62.5 mg of the ET-1 antagonist bosentan. Bosentan 145-153 endothelin 1 Homo sapiens 129-133 33209081-3 2020 Results: Whether ET-1 is present or not in the tumor area, bosentan exerts anti-proliferative effect on breast cancer. Bosentan 59-67 endothelin 1 Homo sapiens 17-21 33209081-4 2020 However, ET-1 and bosentan group showed important inhibitory effect on tumor migration compared to bosentan alone, which can be attributed to increased activity of ET-1 axis in the presence of ET-1. Bosentan 18-26 endothelin 1 Homo sapiens 164-168 33209081-4 2020 However, ET-1 and bosentan group showed important inhibitory effect on tumor migration compared to bosentan alone, which can be attributed to increased activity of ET-1 axis in the presence of ET-1. Bosentan 18-26 endothelin 1 Homo sapiens 164-168 33209081-4 2020 However, ET-1 and bosentan group showed important inhibitory effect on tumor migration compared to bosentan alone, which can be attributed to increased activity of ET-1 axis in the presence of ET-1. Bosentan 99-107 endothelin 1 Homo sapiens 9-13 33209081-4 2020 However, ET-1 and bosentan group showed important inhibitory effect on tumor migration compared to bosentan alone, which can be attributed to increased activity of ET-1 axis in the presence of ET-1. Bosentan 99-107 endothelin 1 Homo sapiens 164-168 33209081-4 2020 However, ET-1 and bosentan group showed important inhibitory effect on tumor migration compared to bosentan alone, which can be attributed to increased activity of ET-1 axis in the presence of ET-1. Bosentan 99-107 endothelin 1 Homo sapiens 164-168 33209081-7 2020 The second major finding was that bosentan inhibited ET-1-mediated effects on tumor proliferation and migration. Bosentan 34-42 endothelin 1 Homo sapiens 53-57 32765401-15 2020 Future studies with bosentan in MS should focus on patients with elevated ET-1 levels in cerebrospinal fluid or blood. Bosentan 20-28 endothelin 1 Homo sapiens 74-78 30563869-8 2019 Endothelin-1 (ET-1) and hypoxia-inducible factor-1alpha (HIF-1alpha) were key mediators of REDD1-driven NETs as demonstrated by their inhibition with bosentan and L-ascorbic acid, respectively. Bosentan 150-158 endothelin 1 Homo sapiens 0-12 28500979-5 2017 The assay was successfully applied to assess the time course of plasma ET-1 concentrations in two human volunteers after co-administration of bosentan and clarithromycin. Bosentan 142-150 endothelin 1 Homo sapiens 71-75 28401480-1 2017 BACKGROUND AND OBJECTIVES: Bosentan is a competitive antagonist on endothelin receptor A and B (ETA and ETB), displacing the endogenous binding partner endothelin-1 (ET-1) from its binding sites. Bosentan 27-35 endothelin 1 Homo sapiens 152-164 28401480-1 2017 BACKGROUND AND OBJECTIVES: Bosentan is a competitive antagonist on endothelin receptor A and B (ETA and ETB), displacing the endogenous binding partner endothelin-1 (ET-1) from its binding sites. Bosentan 27-35 endothelin 1 Homo sapiens 166-170 28401480-10 2017 ET-1 plasma and urine profiles were successfully integrated into the bosentan two-compartment, TMDD model encompassing competition for the same receptor. Bosentan 69-77 endothelin 1 Homo sapiens 0-4 28597546-8 2017 Pharmacological blockade with the dual EDN1 receptor antagonist bosentan decreased cell viability and MAPK activation of U266 and RPMI-8226 cells. Bosentan 64-72 endothelin 1 Homo sapiens 39-43 30261985-6 2018 Here, based on our clinical experience, we provide our recommendations for dose titration schemes for PAH medications that require individualized dosing in adult patients, including agents acting on the endothelin-1 pathway (bosentan and ambrisentan), the prostacyclin pathway (epoprostenol, treprostinil, and selexipag), and the nitric oxide pathway (tadalafil and the soluble guanylate cyclase stimulator riociguat). Bosentan 225-233 endothelin 1 Homo sapiens 203-215 29947542-10 2018 Even though ET-1 levels were low (less than 10 nM levels used under normal growth conditions), blocking of ET receptors with bosentan inhibited the necroptosis pathway and improved the cell migration ability of BMVECs, suggesting that under inflammatory conditions, ET-1 activates PCD pathways in BMVECs even at physiological levels. Bosentan 125-133 endothelin 1 Homo sapiens 266-270 27716320-3 2016 In the present study, we evaluated the ability of endothelin-1 (ET-1) dual receptor antagonists bosentan (BOS) and macitentan (MAC) to antagonize EndoMT in vitro. Bosentan 96-104 endothelin 1 Homo sapiens 50-62 25707716-7 2015 RESULTS: In human dermal microvascular endothelial cells, endothelin 1 induced phosphorylation of Fli-1 at Thr(312) through the sequential activation of c-Abl and protein kinase Cdelta, leading to a decrease in Fli-1 protein levels as well as a decrease in binding of Fli-1 to the target gene promoters, whereas bosentan treatment reversed those effects. Bosentan 312-320 endothelin 1 Homo sapiens 58-70 27189349-3 2016 OBJECTIVE: The present study has been structured to explore the effects of bosentan, an ET-1 antagonist on two-kidneyone- clip: 2K1C method induced hypertension provoked vascular dementia (VaD). Bosentan 75-83 endothelin 1 Homo sapiens 88-92 26111581-2 2015 Remarkably, among the ten PPP-enlisted drugs are three endothelin-1 (ET-1) receptor antagonists (ERA"s: ambrisentan, bosentan and macitentan), which are approved for the treatment of Pulmonary Arterial Hypertension (PAH). Bosentan 117-125 endothelin 1 Homo sapiens 55-67 25593238-9 2015 Macitentan or ACT-132577 antagonized the ability of ET-1 to further induce alpha-SMA expression (p = 0.03), COL-1, and FN synthesis (p = 0.03, p = 0.005); bosentan showed similar effects. Bosentan 155-163 endothelin 1 Homo sapiens 52-56 24071933-0 2014 Improvement of plasma endothelin-1 and nitric oxide in patients with systemic sclerosis by bosentan therapy. Bosentan 91-99 endothelin 1 Homo sapiens 22-34 26090478-3 2015 Endothelin receptors antagonists such as bosentan have beneficial effects on vasoconstriction and fibrosis, but less is known about their potential anti-inflammatory effects. Bosentan 41-49 endothelin 1 Homo sapiens 0-10 25048859-9 2014 ET-1/ETR signalling inhibitor, bosentan, inhibited Gd-induced proliferation and calcification of hMSC. Bosentan 31-39 endothelin 1 Homo sapiens 0-4 24632478-7 2014 The patient fully recovered after intensive treatment and administration of the endothelin receptor antagonist bosentan. Bosentan 111-119 endothelin 1 Homo sapiens 80-90 24193244-10 2014 Bosentan (1E-7 M) significantly attenuated combined ET-1/NE dose-response curves in PA (93.1 +- 47.4 vs. 125.3 +- 41.0%; n = 12; p < 0.001) whereas the effect of sildenafil (1E-5 M) was less pronounced (103.6 +- 20.2%; p < 0.05). Bosentan 0-8 endothelin 1 Homo sapiens 52-59 24071933-1 2014 The aim of this study was to evaluate the effects of bosentan on plasma endothelin-1 (ET-1) and nitric oxide (NO) as pulmonary hypertension (PH)-associated biochemical markers in patients with systemic sclerosis (SSc). Bosentan 53-61 endothelin 1 Homo sapiens 72-84 24071933-1 2014 The aim of this study was to evaluate the effects of bosentan on plasma endothelin-1 (ET-1) and nitric oxide (NO) as pulmonary hypertension (PH)-associated biochemical markers in patients with systemic sclerosis (SSc). Bosentan 53-61 endothelin 1 Homo sapiens 86-90 24071933-6 2014 Plasma ET-1 levels were significantly decreased after 24 weeks of bosentan therapy (p < 0.0001), and ET-1 levels of SSc patients with PH decreased to a level comparable to that in patients without PH. Bosentan 66-74 endothelin 1 Homo sapiens 7-11 24071933-10 2014 Additionally, changes in plasma ET-1 levels may indicate the response to bosentan therapy in SSc patients with PH. Bosentan 73-81 endothelin 1 Homo sapiens 32-36 23696678-8 2013 In the BIRD-1 cohort, serum ET-1 was elevated in all cases at SRC (median healthy controls 0.50 pg/ml; SRC 1.48 pg/ml; P < 0.0005), and increased further with bosentan therapy (1.46 vs. 3.05 pg/ml; t-test P < 0.05). Bosentan 162-170 endothelin 1 Homo sapiens 28-32 23984086-6 2013 The reduction of ET-1 levels in DUs patients in therapy with bosentan confirms the efficacy of this molecule both for treatment and prevention of digital ulcers. Bosentan 61-69 endothelin 1 Homo sapiens 17-21 24015303-5 2013 ET-1 was inhibited by Bosentan, ERK1/2 mitogen activated protein kinase (MAPK) was inhibited by U0126 and p38 MAPK was inhibited by SB203580. Bosentan 22-30 endothelin 1 Homo sapiens 0-4 23359533-9 2013 Bosentan treatment was more effective than TGFbeta blockade in reversing the actions of IFN-gamma, including downregulation of alpha-SMA and TGFbeta2, suggesting that activation of the ET-1 pathway plays a main role in the IFN-gamma responses in HDMECs. Bosentan 0-8 endothelin 1 Homo sapiens 185-189 23509249-6 2013 We then used arterial spin-labeling MRI to noninvasively measure CBF and assess the effect of the administration of the ET-1 antagonist bosentan. Bosentan 136-144 endothelin 1 Homo sapiens 120-124 22265324-0 2013 Relationship between baseline ET-1 plasma levels and outcome in patients with idiopathic pulmonary hypertension treated with bosentan. Bosentan 125-133 endothelin 1 Homo sapiens 30-34 22265324-1 2013 OBJECTIVES: To address if baseline endothelin-1 (ET-1) plasma levels might predict clinical worsening (CW) in patients with idiopathic pulmonary hypertension (IPAH) treated with bosentan. Bosentan 178-186 endothelin 1 Homo sapiens 35-47 22483689-4 2012 The stimulatory effect of ET-1 on beta(2)-adrenoceptor mRNA was prevented by the non-selective ET-A/ET-B receptor antagonist bosentan, indicating that it was mediated via specific ET receptors. Bosentan 125-133 endothelin 1 Homo sapiens 26-30 23053682-1 2012 Bosentan, a dual endothelin receptor antagonist, may reduce blood pressure by blocking the vasoconstrictor effect of endothelin-1. Bosentan 0-8 endothelin 1 Homo sapiens 117-129 21828025-3 2012 CS extract (CSE) increased ET(A) and ET(B) expression in HPASMCs and small intrapulmonary arteries, which was attenuated by bosentan, the ET(A) antagonist BQ123 and the ET(B) antagonist BQ788, and by blocking ET-1 with a monoclonal antibody against ET-1, suggesting a feed-forward mechanism mediated by ET-1 release. Bosentan 124-132 endothelin 1 Homo sapiens 209-213 22561246-6 2012 An antagonist of ET(A), bosentan, prevented the interaction between p9-ET(A) and ET-1 in a concentration-dependent manner. Bosentan 24-32 endothelin 1 Homo sapiens 81-85 21828025-3 2012 CS extract (CSE) increased ET(A) and ET(B) expression in HPASMCs and small intrapulmonary arteries, which was attenuated by bosentan, the ET(A) antagonist BQ123 and the ET(B) antagonist BQ788, and by blocking ET-1 with a monoclonal antibody against ET-1, suggesting a feed-forward mechanism mediated by ET-1 release. Bosentan 124-132 endothelin 1 Homo sapiens 249-253 21828025-3 2012 CS extract (CSE) increased ET(A) and ET(B) expression in HPASMCs and small intrapulmonary arteries, which was attenuated by bosentan, the ET(A) antagonist BQ123 and the ET(B) antagonist BQ788, and by blocking ET-1 with a monoclonal antibody against ET-1, suggesting a feed-forward mechanism mediated by ET-1 release. Bosentan 124-132 endothelin 1 Homo sapiens 249-253 21828025-5 2012 Furthermore, CSE exposure increased the acute ET-1-induced small intrapulmonary artery contraction, which was attenuated by bosentan, BQ123 and BQ788. Bosentan 124-132 endothelin 1 Homo sapiens 46-50 21432755-11 2012 CONCLUSION: Treatment with the endothelin-1 antagonist bosentan is associated with improvements in hemodynamics and clinical outcome in end-stage heart failure patients with PH. Bosentan 55-63 endothelin 1 Homo sapiens 31-43 22558517-9 2012 Plasma ET-1 in hypoxia during the bosentan period was 2.8 times higher than during for both CS and HS. Bosentan 34-42 endothelin 1 Homo sapiens 7-11 21834070-10 2011 Moreover, inhibition of ET-1 signaling by bosentan abolished the TF-mediated fibrotic capacity of HCMFs. Bosentan 42-50 endothelin 1 Homo sapiens 24-28