Biochemical and Biophysical Research Communications

2008

DOI: 10.1016/j.bbrc.2007.11.061

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Over-expression of angiotensin II type 2 receptor (agtr2) decreases collagen accumulation in atherosclerotic plaque

Abhijit Dandapat

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Main Ras Molecules In Atherosclerosis Through the Magnifying1

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Receptores De Angiotensinas1

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Cited by 46 publications

(34 citation statements)

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“…[32][33][34][35] Thus, in accordance with the pertinent literature, our experiments show that this pathway is also one target of VIF-induced modulation of Ang-II-induced vasoconstriction. Because VIF has no effect on ERK 1/2, the ERK pathway is obviously not essential for the vasoregulatory effects of VIF.…”

Section: Discussionsupporting

confidence: 91%

Identification of the Vasoconstriction-Inhibiting Factor (VIF), a Potent Endogenous Cofactor of Angiotensin II Acting on the Angiotensin II Type 2 Receptor

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et al. 2015

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T he renin-angiotensin system and especially the angiotensin peptides play a central role in the pathophysiology of cardiovascular diseases.1,2 Angiotensin peptides are known to play major roles in regulation of the vascular tone and are strongly involved in the pathophysiology of both chronic kidney disease (CKD) 3 and heart failure. 4 The vasoregulatory effects of the angiotensin peptides are mediated by the angiotensin II (Ang-II) type 1 receptor (AT1) receptor, Ang-II type 2 receptor (AT2) receptor, and Mas receptor. Most of the vasoconstrictive effects of angiotensin peptides are mediated by AT1, which is widely distributed in all organs, including adrenal glands, kidney, heart, and vasculature (see Mehta and Griendling 5 for a review). Activation of the AT2 by angiotensin peptides results in vasodilation, nitric oxide release, and Background-The renin-angiotensin system and especially the angiotensin peptides play a central role in blood pressure regulation. Here, we hypothesize that an as-yet unknown peptide is involved in the action of angiotensin II modulating the vasoregulatory effects as a cofactor. Methods and Results-The peptide with vasodilatory properties was isolated from adrenal glands chromatographically.The effects of this peptide were evaluated in vitro and in vivo, and the receptor affinity was analyzed. The plasma concentration in humans was quantified in patients with chronic kidney disease, patients with heart failure, and healthy control subjects. The amino acid sequence of the peptide from bovine adrenal glands was HSSYEDELSEVL EKPNDQAE PKEVTEEVSSKDAAE, which is a degradation product of chromogranin A. The sequence of the peptide isolated from human plasma was HSGFEDELSEVLENQSSQAELKEAVEEPSSKDVME. Both peptides diminished significantly the vasoconstrictive effect of angiotensin II in vitro. Therefore, we named the peptide vasoconstriction-inhibiting factor (VIF). The vasoregulatory effects of VIF are mediated by the angiotensin II type 2 receptor. VIF impairs angiotensin II-induced phosphorylation of the p38 mitogen-activated protein kinase pathway but not of extracellular-regulated kinase 1/2. The vasodilatory effects were confirmed in vivo. The plasma concentration was significantly increased in renal patients and patients with heart failure. Conclusions-VIF is a vasoregulatory peptide that modulates the vasoconstrictive effects of angiotensin II by acting on the angiotensin II type 2 receptor. It is likely that the increase in VIF may serve as a counterregulatory effect to defend against hypertension. The identification of this target may help us to understand the pathophysiology of renal and heart failure and may form a basis for the development of new strategies for the prevention and treatment of cardiovascular disease. inhibition of proliferation and growth. 6,7 The activation of the Mas receptor by angiotensin peptides counteracted many effects of the AT1 receptor such as vasoconstriction. [8][9][10] Among these angiotensin peptides, the physiological and pathophysiological eff...

“…[32][33][34][35] Thus, in accordance with the pertinent literature, our experiments show that this pathway is also one target of VIF-induced modulation of Ang-II-induced vasoconstriction. Because VIF has no effect on ERK 1/2, the ERK pathway is obviously not essential for the vasoregulatory effects of VIF.…”

Section: Discussionsupporting

confidence: 91%

Identification of the Vasoconstriction-Inhibiting Factor (VIF), a Potent Endogenous Cofactor of Angiotensin II Acting on the Angiotensin II Type 2 Receptor

¹

,

²

,

³

et al. 2015

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T he renin-angiotensin system and especially the angiotensin peptides play a central role in the pathophysiology of cardiovascular diseases.1,2 Angiotensin peptides are known to play major roles in regulation of the vascular tone and are strongly involved in the pathophysiology of both chronic kidney disease (CKD) 3 and heart failure. 4 The vasoregulatory effects of the angiotensin peptides are mediated by the angiotensin II (Ang-II) type 1 receptor (AT1) receptor, Ang-II type 2 receptor (AT2) receptor, and Mas receptor. Most of the vasoconstrictive effects of angiotensin peptides are mediated by AT1, which is widely distributed in all organs, including adrenal glands, kidney, heart, and vasculature (see Mehta and Griendling 5 for a review). Activation of the AT2 by angiotensin peptides results in vasodilation, nitric oxide release, and Background-The renin-angiotensin system and especially the angiotensin peptides play a central role in blood pressure regulation. Here, we hypothesize that an as-yet unknown peptide is involved in the action of angiotensin II modulating the vasoregulatory effects as a cofactor. Methods and Results-The peptide with vasodilatory properties was isolated from adrenal glands chromatographically.The effects of this peptide were evaluated in vitro and in vivo, and the receptor affinity was analyzed. The plasma concentration in humans was quantified in patients with chronic kidney disease, patients with heart failure, and healthy control subjects. The amino acid sequence of the peptide from bovine adrenal glands was HSSYEDELSEVL EKPNDQAE PKEVTEEVSSKDAAE, which is a degradation product of chromogranin A. The sequence of the peptide isolated from human plasma was HSGFEDELSEVLENQSSQAELKEAVEEPSSKDVME. Both peptides diminished significantly the vasoconstrictive effect of angiotensin II in vitro. Therefore, we named the peptide vasoconstriction-inhibiting factor (VIF). The vasoregulatory effects of VIF are mediated by the angiotensin II type 2 receptor. VIF impairs angiotensin II-induced phosphorylation of the p38 mitogen-activated protein kinase pathway but not of extracellular-regulated kinase 1/2. The vasodilatory effects were confirmed in vivo. The plasma concentration was significantly increased in renal patients and patients with heart failure. Conclusions-VIF is a vasoregulatory peptide that modulates the vasoconstrictive effects of angiotensin II by acting on the angiotensin II type 2 receptor. It is likely that the increase in VIF may serve as a counterregulatory effect to defend against hypertension. The identification of this target may help us to understand the pathophysiology of renal and heart failure and may form a basis for the development of new strategies for the prevention and treatment of cardiovascular disease. inhibition of proliferation and growth. 6,7 The activation of the Mas receptor by angiotensin peptides counteracted many effects of the AT1 receptor such as vasoconstriction. [8][9][10] Among these angiotensin peptides, the physiological and pathophysiological eff...

“…44 This adds weight to the in vivo animal studies which highlight a role for the AT 2 receptor in the development and progression of atherosclerotic lesions. 16,[38][39][40] However, since at present it is not known for certain whether the G allele is associated with an increase or decrease in AT 2 receptor expression, these data cannot be extrapolated to determine whether an increase in AT 2 receptor expression in a human atherosclerotic lesion would be beneficial or harmful. the ReninAngiotensinAldosterone System (Including other Peptidergic systems)…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II type 2 receptor gene polymorphisms in cardiovascular disease

¹

2009

J Renin Angiotensin Aldosterone Syst

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Considerable progress in our understanding of the role of the angiotensin II type 2 (AT 2 ) receptor in the development of cardiac hypertrophy and coronary artery disease has been achieved using in vitro and in vivo animal models. Our understanding in humans, however, has been hindered by the lack of availability of specific AT 2 receptor agonists and antagonists suitable for human study. Nevertheless, an alternative approach involving genotyping humans for a functional polymorphism within the AT 2 receptor gene (-1332G/A) has been used in several association studies to elucidate the pathogenic role of the AT 2 receptor in cardiovascular disease. Both the A allele and the G allele have independently been associated with left ventricular remodelling. However, the methods of measuring left ventricular mass, sodium balance, age and degree of remodelling appear to influence the outcome. An association of carriers of the G allele and premature coronary artery disease has also been established, particularly in males presenting with stenotic atherosclerosis requiring revascularisation. At the molecular level, it remains unclear as to whether carriers of the G allele express more or fewer AT 2

“…AT2R overexpression in LDLR-knockout mice reduces atherogenesis in the aorta, as well as, expression and activity of MMP-2, MMP-9 and collagen accumulation in atherosclerotic regions [103]. In the same model, the presence of AT2R modulated oxidative stress, by decreasing expression of LOX-1, endothelial NO synthase (eNOS) and heme oxygenase-1 (HO-1) [104].…”

Section: Main Ras Molecules In Atherosclerosis Through the Magnifyingmentioning

confidence: 98%

Involvement of the Renin‐Angiotensin System in Atherosclerosis

2017

Renin-Angiotensin System - Past, Present and Future

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The renin-angiotensin system (RAS) is a well known for its role in the regulation of the blood pressure (BP). Angiotensin II (Ang II), the main mediator of the RAS, may act either, as a systemic molecule or a locally produced factor. Within the vessel wall it has significant proinflammatory role by inducing the oxidative stress, secretion of inflammatory cytokines and adhesion molecules. Ang II could trigger proliferation of vascular smooth muscle cells (VSMC) and its migration to the outer layer of the vessel wall. It could induce the release of matrix metalloproteinase (MMPs), from human VSMC and thus increase susceptibility to rupture of atherosclerotic lesions. Binding of Ang II to AT1R/AT2R could have opposing actions in vascular injury. The ACE2/Ang (1-7)/Mas axis of the RAS also opposes the unfavourable actions of ACE/Ang II/ATR1 axis. Inhibition of RAS could reduce inflammation-associated processes in vasculature, independently of lowering BP. RAS is significantly modulated by the genes coding for this system. Certain genetic variants (SNPs) in the RAS genes have been denoted as the functional ones and have been associated with hypertension, cardiovascular phenotypes and atherosclerosis. Also, the genetic components of the RAS interfere with the regulators of gene expression by microRNAs (miRs).

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