Angiotensin-(1–7) abrogates mitogen-stimulated proliferation of cardiac fibroblasts

McCollum, LaTronya; Gallagher, Patricia E.; Tallant, E. Ann

doi:10.1016/j.peptides.2012.01.020

Cited by 49 publications

(43 citation statements)

References 61 publications

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“…In contrast to the present study, Ferreira et al showed an improved cardiac function, indicated by elevated dp/dt anddp/dt and furthermore, an attenuation of the isoproterenolinduced cardiac fibrosis in transgenic rats. Previous studies also indicated an antifibrotic action of Ang(1-7) in vitro and in vivo (Santos et al, 2004;Ferreira et al, 2010;Dong et al, 2012;McCollum et al, 2012;Acuña et al, 2014). In contrast to these findings, the present study revealed no antifibrotic effect of Ang(1-7) in a transgenic rat model.…”

Section: Discussioncontrasting

confidence: 87%

“…Several studies exist, revealing a cardioprotective role of ACE2 and Ang(1-7) (Ferreira et al, 2001;Pei et al, 2010;Johnson et al, 2011;Dong et al, 2012;Feng et al, 2012;McCollum et al, 2012). In contrast to the above mentioned proarrhythmic effect of high Ang(1-7) concentrations, Ferreira et al detected reduced cardiac arrhythmias induced by ischemia/reperfusion associated with low dose Ang(1-7) if acutely administered (Ferreira et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

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Effect of Angiotensin (1-7) on Heart Function in an Experimental Rat Model of Obesity

Blanke¹,

Schlegel²,

Salameh³

et al. 2016

Thorac cardiovasc Surg

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Aim: Obesity is a risk factor for the development of cardiovascular diseases. Recently it was shown that overexpression of the Mas-receptor antagonist angiotensin(1-7) could prevent from diet-induced obesity. However, it remained unclear whether diet-induced obesity and angiotensin(1-7) overexpression might also have effects on the cardiovascular system in these rats.Methods: Twenty three male Sprague Dawley rats were fed with standard chow (SD+chow, n = 5) or a cafeteria diet (SD+CD, n = 6) for 5 months. To investigate the effect of angiotensin(1-7) transgenic rats, expressing an angiotensin(1-7)-producing fusion protein in testis were used. These transgenic rats also received a 5 month's feeding period with either chow (TGR+chow, n = 6) or cafeteria diet (TGR+CD, n = 6), respectively. Hemodynamic measurements (pressure-volume loops) were carried out to assess cardiac function and blood pressure. Subsequently, hearts were explanted and investigated according to the Langendorff technique. Furthermore, cardiac remodeling in these animals was investigated histologically.Results: After 5 months cafeteria diet feeding rats showed a significantly increased body weight, which could be prevented in transgenic rats. However, there was no effect on cardiac performance after cafeteria diet in non-transgenic and transgenic rats. Moreover, overexpression of angiotensin(1-7) deteriorated cardiac contractility as indicated by impaired dp/dt. Furthermore, histological analysis revealed that cafeteria diet led to myocardial fibrosis in both, control and transgenic rats and this was not inhibited by an overproduction of angiotensin(1-7). Conclusion:These results indicate that an overexpression of circulating angiotensin(1-7) prevents a cafeteria diet-induced increase in body weight, but does not affect cardiac performance in this experimental rat model of obesity. Furthermore, overexpression of angiotensin(1-7) alone resulted in an impairment of cardiac function.

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Section: Discussioncontrasting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Effect of Angiotensin (1-7) on Heart Function in an Experimental Rat Model of Obesity

Blanke¹,

Schlegel²,

Salameh³

et al. 2016

Thorac cardiovasc Surg

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show abstract

“…Ang-(1-7) was generally thought to inhibit the proliferation of some cell types, including tumor cells, vascular smooth muscle cells and cultured neonatal cardiac myocytes (16,17); but in some other cell types, such as fibroblasts, epidermal stem cells, keratinocytes and hematopoietic progenitors, Ang-(1-7) stimulates cell proliferation (18,19). Thus, whether Ang- (1-7) is an antiproliferative or proproliferative agent for particular tumors or host cells may be an important consideration for understanding the role of RAS in the carcinogenic process and the application of RAS blockade in anticancer therapy.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-(1–1) Suppresses Hepatocellular Carcinoma Growth and Angiogenesis via Complex Interactions of Angiotensin II Type 1 Receptor, Angiotensin II Type 2 Receptor and Mas Receptor

Liu

Wang

et al. 2015

Mol Med

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We recently confirmed that angiotensin II (Ang II) type 1 receptor (AT 1 R) was overexpressed in hepatocellular carcinoma tissue using a murine hepatoma model. Angiotensin(Ang)-(1-7) has been found beneficial in ameliorating lung cancer and prostate cancer. Which receptor of Ang-(1-7) is activated to mediate its effects is much speculated. This study was designed to investigate the effects of Ang-(1-7) on hepatocellular carcinoma, as well as the probable mechanisms. H22 hepatoma-bearing mice were randomly divided into five groups for treatment: mock group, low-dose Ang-(1-7), high-dose Ang-(1-7), high-dose Ang-(1-7) + A779 and high-dose Ang-(1-7) + PD123319. Ang-(1-7) treatment inhibited tumor growth time-and dose-dependently by arresting tumor proliferation and promoting tumor apoptosis as well as inhibiting tumor angiogenesis. The effects of Ang-(1-7) on tumor proliferation and apoptosis were reversed by coadministration with A779 or PD123319, whereas the effects on tumor angiogenesis were completely reversed by A779 but not by PD123319. Moreover, Ang-(1-7) downregulated AT 1 R mRNA, upregulated mRNA levels of Ang II type 2 receptor (AT 2 R) and Mas receptor (MasR) and p38-MAPK phosphorylation and suppressed H22 cell-endothelial cell communication. Thus, Ang-(1-7) administration suppresses hepatocellular carcinoma via complex interactions of AT 1 R, AT 2 R and MasR and may provide a novel and promising approach for the treatment of hepatocellular carcinoma.

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“…In vitro studies in both adult and neonatal rat cardiac fibroblasts have demonstrated that Ang-(1-7) inhibits proliferation and collagen production [57,58]. In neonatal rat cardiac fibroblasts, Ang-(1-7) achieved this via reduced AngII-mediated phospho-ERK1 (extracellular-signal-regulated kinase 1) and -ERK2 levels and increasing DUSP1 (dual-specificity phosphatase 1) activity, which in turn reduced MAPK (mitogenactivated protein kinase) activity and prevented production of proproliferative prostaglandin-2 [58].…”

Section: Effects Of Ang-(1-7)mentioning

confidence: 99%

Angiotensin-(1–7) and angiotensin-(1–9): function in cardiac and vascular remodelling

et al. 2014

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The RAS (renin-angiotensin system) is integral to cardiovascular physiology; however, dysregulation of this system largely contributes to the pathophysiology of CVD (cardiovascular disease). It is well established that AngII (angiotensin II), the main effector of the RAS, engages the AT1R (angiotensin type 1 receptor) and promotes cell growth, proliferation, migration and oxidative stress, all processes which contribute to remodelling of the heart and vasculature, ultimately leading to the development and progression of various CVDs, including heart failure and atherosclerosis. The counter-regulatory axis of the RAS, which is centred on the actions of ACE2 (angiotensin-converting enzyme 2) and the resultant production of Ang-(1-7) [angiotensin-(1-7)] from AngII, antagonizes the actions of AngII via the receptor Mas, thereby providing a protective role in CVD. More recently, another ACE2 metabolite, Ang-(1-9) [angiotensin-(1-9)], has been reported to be a biologically active peptide within the counter-regulatory axis of the RAS. The present review will discuss the role of the counter-regulatory RAS peptides Ang-(1-7) and Ang-(1-9) in the cardiovascular system, with a focus on their effects in remodelling of the heart and vasculature.

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Angiotensin-(1–7) abrogates mitogen-stimulated proliferation of cardiac fibroblasts

Cited by 49 publications

References 61 publications

Effect of Angiotensin (1-7) on Heart Function in an Experimental Rat Model of Obesity

Effect of Angiotensin (1-7) on Heart Function in an Experimental Rat Model of Obesity

Angiotensin-(1–1) Suppresses Hepatocellular Carcinoma Growth and Angiogenesis via Complex Interactions of Angiotensin II Type 1 Receptor, Angiotensin II Type 2 Receptor and Mas Receptor

Angiotensin-(1–7) and angiotensin-(1–9): function in cardiac and vascular remodelling

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