Angiotensin 1-7 Inhibits Allergic Inflammation, Via The Mas Receptor, Through Suppression Of ERK1/2 And NF-kB Dependent Pathways

El-Hashim, Ahmed Z.; Renno, Waleed M.; Abduo, Heba; Akhtar, Saghir; Benter, İbrahim F.

doi:10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5647

Cited by 4 publications

(10 citation statements)

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“…() showed that a lentiviral‐mediated pulmonary overexpression of Ang‐(1‐7) prevented pulmonary fibrosis after bleomycin administration, resulting in a significant decrease in mRNA levels of TGF‐β and some pro‐inflammatory cytokines. More recently, Ang‐(1‐7) attenuated OVA‐induced leukocyte influx in airway spaces, perivascular and peribronchial inflammation in a short‐term model of allergic asthma (El‐Hashim et al ., ). Altogether, these results suggest that Ang‐(1‐7) may depress leukocyte migration, cytokine expression and release during the onset of chronic lung allergic inflammation.…”

Section: Discussionmentioning

confidence: 98%

“…Moreover, as observed by El‐Hashim et al . (), treatment with Ang‐(1‐7) resulted in a significant reduction in peribronchial and perivascular fibrosis and inflammation in an short‐term model of allergic asthma. Additionally, Klein et al .…”

Section: Discussionmentioning

confidence: 99%

“…There is one published report that Ang‐(1‐7) presents an anti‐inflammatory and anti‐fibrotic action in a model of short‐term allergic lung inflammation (El‐Hashim et al ., ). More recently, we have shown that AVE 0991 attenuated pulmonary remodelling in a model of long‐term allergic lung inflammation (Rodrigues‐Machado et al ., ).…”

Section: Introductionmentioning

confidence: 97%

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Angiotensin‐(1‐7) attenuates airway remodelling and hyperresponsiveness in a model of chronic allergic lung inflammation

Magalhães

Rodrigues-Machado

Motta‐Santos

et al. 2015

British J Pharmacology

110

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BACKGROUND AND PURPOSEA long-term imbalance between pro-and anti-inflammatory mediators leads to airway remodelling, which is strongly correlated to most of the symptoms, severity and progression of chronic lung inflammation. The Angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis of the renin-angiotensin system is associated with attenuation of acute and chronic inflammatory processes. In this study, we investigated the effects of Ang-(1-7) treatment in a model of chronic allergic lung inflammation. EXPERIMENTAL APPROACHMice were sensitized to ovalbumin (OVA; 4 injections over 42 days, 14 days apart) and were challenged three times per week (days 21-46). These mice received Ang-(1-7) (1 μg·h −1 , s.c.) by osmotic mini-pumps, for the last 28 days. Histology and morphometric analysis were performed in left lung and right ventricle. Airway responsiveness to methacholine, analysis of Ang-(1-7) levels (RIA), collagen I and III (qRT-PCR), ERK1/2 and JNK (Western blotting), IgE (ELISA), cytokines and chemokines (ELISA multiplex), and immunohistochemistry for Mas receptors were performed. KEY RESULTSInfusion of Ang-(1-7) in OVA-sensitized and challenged mice decreased inflammatory cell infiltration and collagen deposition in the airways and lung parenchyma, and prevented bronchial hyperresponsiveness. These effects were accompanied by decreased IgE and ERK1/2 phosphorylation, and decreased pro-inflammatory cytokines. Mas receptors were detected in the epithelium and bronchial smooth muscle, suggesting a site in the lung for the beneficial actions of Ang-(1-7).

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

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Angiotensin‐(1‐7) attenuates airway remodelling and hyperresponsiveness in a model of chronic allergic lung inflammation

Magalhães

Rodrigues-Machado

Motta‐Santos

et al. 2015

British J Pharmacology

110

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“…Indeed cAng-(1-7) and dKcAng-(1-7) function fundamentally differently. cAng-(1-7) stimulates MAS, whereas dKcAng-(1-7) acts via AT2, which receptor seems to heterodimerize with AT1, thereby inhibiting AT1 receptor signaling (14,44). Apparently these functional differences may cause the differential effects on inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…In mice with renal ischemia-reperfusion injury Ang-(1-7) infusion aggravated the inflammatory response, whereas kidney injury in MAS-deficient mice was less severe (15). In contrast, an anti-inflammatory effect of Ang-(1-7) was reported in lungs of mice with experimental asthma by ovalbumin-induced allergic lung inflammation and antigen-induced arthritis (8,14). In both animal models MAS activation attenuated the inflammatory response by decreasing neutrophil accumulation, whereas in mice deficient for MAS arthritis was aggravated because of an increased influx of neutrophils and proinflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

Agonists of MAS oncogene and angiotensin II type 2 receptors attenuate cardiopulmonary disease in rats with neonatal hyperoxia-induced lung injury

Wagenaar

Laghmani

Fidder

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

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Stimulation of MAS oncogene receptor (MAS) or angiotensin (Ang) receptor type 2 (AT2) may be novel therapeutic options for neonatal chronic lung disease (CLD) by counterbalancing the adverse effects of the potent vasoconstrictor angiotensin II, consisting of arterial hypertension (PAH)-induced right ventricular hypertrophy (RVH) and pulmonary inflammation. We determined the cardiopulmonary effects in neonatal rats with CLD of daily treatment during continuous exposure to 100% oxygen for 10 days with specific ligands for MAS [cyclic Ang-(1-7); 10-50 μg·kg(-1)·day(-1)] and AT2 [dKcAng-(1-7); 5-20 μg·kg(-1)·day(-1)]. Parameters investigated included lung and heart histopathology, fibrin deposition, vascular leakage, and differential mRNA expression in the lungs of key genes involved in the renin-angiotensin system, inflammation, coagulation, and alveolar development. We investigated the role of nitric oxide synthase inhibition with N(ω)-nitro-l-arginine methyl ester (25 mg·kg(-1)·day(-1)) during AT2 agonist treatment. Prophylactic treatment with agonists for MAS or AT2 for 10 days diminished cardiopulmonary injury by reducing alveolar septum thickness and medial wall thickness of small arterioles and preventing RVH. Both agonists attenuated the pulmonary influx of inflammatory cells, including macrophages (via AT2) and neutrophils (via MAS) but did not reduce alveolar enlargement and vascular alveolar leakage. The AT2 agonist attenuated hyperoxia-induced fibrin deposition. In conclusion, stimulation of MAS or AT2 attenuates cardiopulmonary injury by reducing pulmonary inflammation and preventing PAH-induced RVH but does not affect alveolar and vascular development in neonatal rats with experimental CLD. The beneficial effects of AT2 activation on experimental CLD were mediated via a NOS-independent mechanism.

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Suppressing inflammation by inhibiting the NF‐κB pathway contributes to the neuroprotective effect of angiotensin‐(1‐7) in rats with permanent cerebral ischaemia

Jiang

Guo

et al. 2012

British J Pharmacology

141

130

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BACKGROUND AND PURPOSEAngiotensin-(1-7) [Ang-(1-7)] has anti-inflammatory effects in peripheral organs, but its effects in ischaemic stroke are unclear as yet. We investigated whether its anti-inflammatory effect contributes to the neuroprotection induced by Ang-(1-7) in a rat model of permanent middle cerebral artery occlusion (pMCAO). EXPERIMENTAL APPROACHWe infused Ang-(1-7), Mas receptor antagonist A-779, angiotensin II type 2 receptor antagonist PD123319 or artificial CSF into the right lateral ventricle of male Sprague-Dawley rats from 48 h before onset of pMCAO until the rats were killed. Twenty-four hours after pMCAO, the neuroprotective effect of Ang-(1-7) was analysed by evaluating infarct volume and neurological deficits. The levels of oxidative stress were detected by spectrophotometric assay. The activation of NF-kB was assessed by Western blot and immunohistochemistry analysis. The level of COX-2 was tested by Western blot analysis and concentrations of pro-inflammatory cytokines were measured by ELISA. KEY RESULTSInfusion of Ang-(1-7), i.c.v., significantly reduced infarct volume and improved neurological deficits. It decreased the levels of oxidative stress and suppressed NF-kB activity, which was accompanied by a reduction of pro-inflammatory cytokines and COX-2 in the peri-infarct regions. These effects of Ang-(1-7) were reversed by A-779 but not by PD123319. Additionally, infusion of A-779 alone increased oxidative stress levels and enhanced NF-kB activity, which was accompanied by an up-regulation of pro-inflammatory cytokines and COX-2. CONCLUSION AND IMPLICATIONSOur findings indicate that suppressing NF-kB dependent pathway via Mas receptor may represent one mechanism that contributes to the anti-inflammatory effects of Ang-(1-7) in rats with pMCAO.Abbreviations aCSF, artificial CSF; Ang II, angiotensin II; Ang-(1-7), angiotensin-(1-7); CBF, cerebral blood flow; MDA, malondialdehyde; pMCAO, permanent middle cerebral artery occlusion; RAS, renin-angiotensin system; ROS, reactive oxygen species; SOD, superoxide dismutase BJP British Journal of Pharmacology

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Angiotensin 1-7 Inhibits Allergic Inflammation, Via The Mas Receptor, Through Suppression Of ERK1/2 And NF-kB Dependent Pathways

Cited by 4 publications

References 0 publications

Angiotensin‐(1‐7) attenuates airway remodelling and hyperresponsiveness in a model of chronic allergic lung inflammation

Angiotensin‐(1‐7) attenuates airway remodelling and hyperresponsiveness in a model of chronic allergic lung inflammation

Agonists of MAS oncogene and angiotensin II type 2 receptors attenuate cardiopulmonary disease in rats with neonatal hyperoxia-induced lung injury

Suppressing inflammation by inhibiting the NF‐κB pathway contributes to the neuroprotective effect of angiotensin‐(1‐7) in rats with permanent cerebral ischaemia

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