Opposing actions of angiotensins on angiogenesis

Machado, R. D. P.; Santos, Robson A.S.; Andrade, Sílvia Passos

doi:10.1016/s0024-3205(99)00562-7

Cited by 86 publications

(66 citation statements)

References 34 publications

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“…Antiangiogenic properties of Ang-(1-7), first described by Machado et al, 58,59 and those reported by us on protein synthesis 35,60 endow this peptide with antitumoral properties since Gallagher and Tallant 61 showed that Ang-(1-7) inhibits growth in 3 human lung cancer cell lines (human adenocarcinoma SK-LU-1, A549 cells, and non-small lung cancer SK-MES-1 cells). Treatment with Ang-(1-7) resulted in both a dose-and time-dependent reduction in serum-stimulated DNA synthesis in all 3 of the cell lines, with an IC 50 in the subnanomolar range.…”

Section: An Additional Perspectivementioning

confidence: 87%

Angiotensin-Converting Enzyme 2 and Angiotensin-(1-7)

2006

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Abstract-This lecture summarizes the chronology and rationale that led to the discovery of angiotensin-(1-7) as a hormone that, in its own right, opposes the vasoconstrictor and proliferative actions of angiotensin II. The work discussed here additionally analyzes the newest findings on angiotensin-converting enzyme 2, the angiotensin-converting enzyme homologue that efficiently hydrolyzes angiotensin II into angiotensin-(1-7). Both components of this system may significantly influence our future perspective of the role of the renin-angiotensin system, not just in terms of its role in the regulation of cardiovascular and renal function but, moreover, as regulators of a vast array of disease processes in which inflammation and immune mechanisms play a role.

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Section: An Additional Perspectivementioning

confidence: 87%

Angiotensin-Converting Enzyme 2 and Angiotensin-(1-7)

2006

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“…Recent studies have shown that at a local tissue level, the components of the RAS influence tumor growth by changing its microenvironment [6,7]. Angiotensin-(1 -7) [Ang-(1 -7)] is an endogenous peptide hormone that functions as a vasodilator [8] with antihypertensive [9], antiproliferative [10][11][12] and antiangiogenic properties [13]. The formation of Ang-(1 -7) from Ang I requires the action of three tissue endopeptidases: prolyl endopeptidase, neutral endopeptidase and thimet oligopeptidase [14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Effects on Cell Viability and on Apoptosis in Tumoral (MCF-7) and in Normal (MCF10A) Epithelial Breast Cells after Human Chorionic Gonadotropin and Derivated-Angiotensin Peptides Treatments

Noronha¹,

Bernardo²,

Barros³

et al. 2013

JCT

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Angiotensin-(1 -7) ] is an endogenous heptapeptide hormone of the renin-angiotensin system that has antiproliferative properties. The aim of this work was to evaluate the anti-proliferative and pro-apoptotic properties of Ang-(1 -7) and of Ang-(1 -7)-substituents 9-fluorenylmethyloxycarbonyl (Fmoc) e Ang II-derivatives containing the TOAC (2,2,6,6-tetramethylpiperidine-N-oxyl-4-amino-4-carboxylic acid) in normal (MCF10A) and in tumoral (MCF7) epithelial mammary cell lines. Both cell lines received an hCG and angiotensin peptides 24-hour treatment, in combination or alone followed by cell viability, apoptosis and cell cycle assays performed by flow cytometer (GUAVA). After hCG, Ang-(1 -7), hCG + Ang-(1 -7) and hCG + Ang-(1 -7)-Fmoc treatments, MCF7 displayed cell viability decrease and mid-apoptosis increase. We also observed cell viability decrease in MCF10A after Ang-(1 -7), Ang-(1 -7) Fmoc and hCG + AngII Toac treatments. These cells had an increase in late apoptosis and necrosis after AngII Toac, hCG + Ang-(1 -7) and hCG + Ang-(1 -7)-Fmoc treatments. Regarding the cell cycle analysis, we did not observed any changes in cell cycle phases. In summary, cell viability was decreased and apoptosis (initial, mid and late) was increased after hCG and/or Ang-(1 -7) peptides treatments. These results point out hCG and Ang-(1 -7) as effective compounds to inhibit cell proliferation, since they decrease cell viability and increase apoptosis in both normal and in tumoral breast cells, being the effect more pronounced in the tumoral cell line. Our results support the idea of investigating more closely the putative use of these compounds as novel therapeutic agents for breast cancer.

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“…It has been demonstrated that Ang-(1-7) acts as a counter-regulatory hormone to Ang II, limiting its pressor, proliferative, and angiogenic actions. [12][13][14] However, very little is known about the role of Ang-(1-7) in the regulation of hemostasis. In contrast to Ang I, II, and III, Ang-(1-7) does not induce TF and PAI-1 mRNA expression in cultured rat aortic endothelial cells, 15 indicating that it should not promote thrombosis in vivo.…”

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confidence: 99%

Antithrombotic Effect of Captopril and Losartan Is Mediated by Angiotensin-(1-7)

et al. 2002

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Abstract-It is well established that renin-angiotensin system blockers exert NO/prostacyclin-dependent antithrombotic effects. Because some beneficial effects of these drugs are mediated by angiotensin (Ang)-(1-7), in the present study we examined if their antithrombotic action could be mediated by Ang-(1-7). Intravenous infusion of Ang-(1-7) (1, 10, or 100 pmol/kg per minute for 2 hours) into rats developing venous thrombosis caused 50% to 70% reduction of the thrombus weight. This effect was dose-dependently reversed by cotreatment with A-779 (selective Ang- [1][2][3][4][5][6][7] receptor antagonist) or EXP 3174 (angiotensin type 1 receptor antagonist) but not by PD 123,319 (angiotensin type 2 receptor antagonist). Similarly, the antithrombotic effects of captopril (ACE inhibitor) and losartan (angiotensin type 1 receptor blocker) were attenuated by A-779 in a dose-dependent manner. The effect of Ang-(1-7) was completely abolished by concomitant administration of NO synthase inhibitor (N G -nitro-L-arginine methyl ester) and prostacyclin synthesis inhibitor (indomethacin), as has been shown previously for captopril and losartan. Thus, the antithrombotic effect of renin-angiotensin system blockers involves Ang-(1-7)-evoked release of NO and prostacyclin. (Hypertension. 2002;40:774-779.)

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Opposing actions of angiotensins on angiogenesis

Cited by 86 publications

References 34 publications

Angiotensin-Converting Enzyme 2 and Angiotensin-(1-7)

Angiotensin-Converting Enzyme 2 and Angiotensin-(1-7)

Effects on Cell Viability and on Apoptosis in Tumoral (MCF-7) and in Normal (MCF10A) Epithelial Breast Cells after Human Chorionic Gonadotropin and Derivated-Angiotensin Peptides Treatments

Antithrombotic Effect of Captopril and Losartan Is Mediated by Angiotensin-(1-7)

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