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Ang-(1-7) is an endogenous β-arrestin-biased agonist of the AT1 receptor with protective action in cardiac hypertrophy (2017)

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  • Unidade: FMRP
  • DOI: 10.1038/s41598-017-12074-3
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  • Language: Inglês
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    • ABNT

      TEIXEIRA, Larissa B.; PARREIRAS-E-SILVA, Lucas T.; BRUDER-NASCIMENTO, Thiago; et al. Ang-(1-7) is an endogenous β-arrestin-biased agonist of the AT1 receptor with protective action in cardiac hypertrophy. Scientific Reports, London, v. 7, n. 1, 2017. Disponível em: < http://dx.doi.org/10.1038/s41598-017-12074-3 > DOI: 10.1038/s41598-017-12074-3.
    • APA

      Teixeira, L. B., Parreiras-e-Silva, L. T., Bruder-Nascimento, T., Duarte, D. A., Simões, S. C., Costa, R. M., et al. (2017). Ang-(1-7) is an endogenous β-arrestin-biased agonist of the AT1 receptor with protective action in cardiac hypertrophy. Scientific Reports, 7( 1). doi:10.1038/s41598-017-12074-3
    • NLM

      Teixeira LB, Parreiras-e-Silva LT, Bruder-Nascimento T, Duarte DA, Simões SC, Costa RM, Rodríguez DY, Ferreira PAB, Silva CAA da, Abrao EP, Oliveira EB de, Bouvier M, Tostes R de CA, Costa Neto CM. Ang-(1-7) is an endogenous β-arrestin-biased agonist of the AT1 receptor with protective action in cardiac hypertrophy [Internet]. Scientific Reports. 2017 ; 7( 1):Available from: http://dx.doi.org/10.1038/s41598-017-12074-3
    • Vancouver

      Teixeira LB, Parreiras-e-Silva LT, Bruder-Nascimento T, Duarte DA, Simões SC, Costa RM, Rodríguez DY, Ferreira PAB, Silva CAA da, Abrao EP, Oliveira EB de, Bouvier M, Tostes R de CA, Costa Neto CM. Ang-(1-7) is an endogenous β-arrestin-biased agonist of the AT1 receptor with protective action in cardiac hypertrophy [Internet]. Scientific Reports. 2017 ; 7( 1):Available from: http://dx.doi.org/10.1038/s41598-017-12074-3

    Referências citadas na obra
    Karnik, S. S. et al. International Union of Basic and Clinical Pharmacology. XCIX. Angiotensin Receptors: Interpreters of Pathophysiological Angiotensinergic Stimuli [corrected]. Pharmacological reviews 67, 754–819, https://doi.org/10.1124/pr.114.010454 (2015).
    Kobori, H., Nangaku, M., Navar, L. G. & Nishiyama, A. The intrarenal renin-angiotensin system: from physiology to the pathobiology of hypertension and kidney disease. Pharmacological reviews 59, 251–287, https://doi.org/10.1124/pr.59.3.3 (2007).
    Santos, R. A., Brosnihan, K. B., Jacobsen, D. W., DiCorleto, P. E. & Ferrario, C. M. Production of angiotensin-(1-7) by human vascular endothelium. Hypertension 19, II56–61 (1992).
    Ferrario, C. M. & Chappell, M. C. A new myocardial conversion of angiotensin I. Current opinion in cardiology 9, 520–526 (1994).
    Pereira, M. G. et al. Angiotensin II-independent angiotensin-(1-7) formation in rat hippocampus: involvement of thimet oligopeptidase. Hypertension 62, 879–885, https://doi.org/10.1161/HYPERTENSIONAHA.113.01613 (2013).
    Santos, R. A. Angiotensin-(1-7). Hypertension 63, 1138–1147, https://doi.org/10.1161/HYPERTENSIONAHA.113.01274 (2014).
    Porrello, E. R., Delbridge, L. M. & Thomas, W. G. The angiotensin II type 2 (AT2) receptor: an enigmatic seven transmembrane receptor. Front Biosci (Landmark Ed) 14, 958–972 (2009).
    Costa-Neto, C. M. et al. Non-canonical signalling and roles of the vasoactive peptides angiotensins and kinins. Clinical science 126, 753–774, https://doi.org/10.1042/CS20130414 (2014).
    de Gasparo, M., Catt, K. J., Inagami, T., Wright, J. W. & Unger, T. International union of pharmacology. XXIII. The angiotensin II receptors. Pharmacological reviews 52, 415–472 (2000).
    Ferrario, C. M. Angiotension-(1-7) and antihypertensive mechanisms. Journal of nephrology 11, 278–283 (1998).
    Santos, R. A. et al. Angiotensin-(1-7) is an endogenous ligand for the G protein-coupled receptor Mas. Proceedings of the National Academy of Sciences of the United States of America 100, 8258–8263, https://doi.org/10.1073/pnas.1432869100 (2003).
    Young, D., Waitches, G., Birchmeier, C., Fasano, O. & Wigler, M. Isolation and characterization of a new cellular oncogene encoding a protein with multiple potential transmembrane domains. Cell 45, 711–719 (1986).
    Rabin, M. et al. Human ros1 and mas1 oncogenes located in regions of chromosome 6 associated with tumor-specific rearrangements. Oncogene research 1, 169–178 (1987).
    Pena Silva, R. A. et al. Angiotensin 1-7 reduces mortality and rupture of intracranial aneurysms in mice. Hypertension 64, 362–368, https://doi.org/10.1161/HYPERTENSIONAHA.114.03415 (2014).
    Noda, K., Saad, Y. & Karnik, S. S. Interaction of Phe8 of angiotensin II with Lys199 and His256 of AT1 receptor in agonist activation. The Journal of biological chemistry 270, 28511–28514 (1995).
    Holloway, A. C. et al. Side-chain substitutions within angiotensin II reveal different requirements for signaling, internalization, and phosphorylation of type 1A angiotensin receptors. Molecular pharmacology 61, 768–777 (2002).
    Wei, H., Ahn, S., Barnes, W. G. & Lefkowitz, R. J. Stable interaction between beta-arrestin 2 and angiotensin type 1A receptor is required for beta-arrestin 2-mediated activation of extracellular signal-regulated kinases 1 and 2. The Journal of biological chemistry 279, 48255–48261, https://doi.org/10.1074/jbc.M406205200 (2004).
    Violin, J. D. et al. Selectively engaging beta-arrestins at the angiotensin II type 1 receptor reduces blood pressure and increases cardiac performance. The Journal of pharmacology and experimental therapeutics 335, 572–579, https://doi.org/10.1124/jpet.110.173005 (2010).
    Gironacci, M. M., Coba, M. P. & Pena, C. Angiotensin-(1-7) binds at the type 1 angiotensin II receptors in rat renal cortex. Regulatory peptides 84, 51–54 (1999).
    Rowe, B. P., Saylor, D. L., Speth, R. C. & Absher, D. R. Angiotensin-(1-7) binding at angiotensin II receptors in the rat brain. Regulatory peptides 56, 139–146 (1995).
    Clark, M. A., Tallant, E. A. & Diz, D. I. Downregulation of the AT1A receptor by pharmacologic concentrations of Angiotensin-(1-7). Journal of cardiovascular pharmacology 37, 437–448 (2001).
    Bosnyak, S. et al. Relative affinity of angiotensin peptides and novel ligands at AT1 and AT2 receptors. Clinical science 121, 297–303, https://doi.org/10.1042/CS20110036 (2011).
    AbdAlla, S., Abdel-Baset, A., Lother, H., el Massiery, A. & Quitterer, U. Mesangial AT1/B2 receptor heterodimers contribute to angiotensin II hyperresponsiveness in experimental hypertension. Journal of molecular neuroscience: MN 26, 185–192, https://doi.org/10.1385/JMN:26:2-3:185 (2005).
    Kostenis, E. et al. G-protein-coupled receptor Mas is a physiological antagonist of the angiotensin II type 1 receptor. Circulation 111, 1806–1813, https://doi.org/10.1161/01.CIR.0000160867.23556.7D (2005).
    Canals, M., Jenkins, L., Kellett, E. & Milligan, G. Up-regulation of the angiotensin II type 1 receptor by the MAS proto-oncogene is due to constitutive activation of Gq/G11 by MAS. The Journal of biological chemistry 281, 16757–16767, https://doi.org/10.1074/jbc.M601121200 (2006).
    Santos, E. L. et al. Functional rescue of a defective angiotensin II AT1 receptor mutant by the Mas protooncogene. Regulatory peptides 141, 159–167, https://doi.org/10.1016/j.regpep.2006.12.030 (2007).
    Tesanovic, S., Vinh, A., Gaspari, T. A., Casley, D. & Widdop, R. E. Vasoprotective and atheroprotective effects of angiotensin (1-7) in apolipoprotein E-deficient mice. Arteriosclerosis, thrombosis, and vascular biology 30, 1606–1613, https://doi.org/10.1161/ATVBAHA.110.204453 (2010).
    Raffai, G., Durand, M. J. & Lombard, J. H. Acute and chronic angiotensin-(1-7) restores vasodilation and reduces oxidative stress in mesenteric arteries of salt-fed rats. American journal of physiology. Heart and circulatory physiology 301, H1341–1352, https://doi.org/10.1152/ajpheart.00202.2011 (2011).
    Marullo, S. & Bouvier, M. Resonance energy transfer approaches in molecular pharmacology and beyond. Trends in pharmacological sciences 28, 362–365, https://doi.org/10.1016/j.tips.2007.06.007 (2007).
    Gales, C. et al. Probing the activation-promoted structural rearrangements in preassembled receptor-G protein complexes. Nature structural & molecular biology 13, 778–786, https://doi.org/10.1038/nsmb1134 (2006).
    Lee, C. H., Park, D., Wu, D., Rhee, S. G. & Simon, M. I. Members of the Gq alpha subunit gene family activate phospholipase C beta isozymes. The Journal of biological chemistry 267, 16044–16047 (1992).
    Wu, D., Katz, A., Lee, C. H. & Simon, M. I. Activation of phospholipase C by alpha 1-adrenergic receptors is mediated by the alpha subunits of Gq family. The Journal of biological chemistry 267, 25798–25802 (1992).
    Steinberg, S. F. Structural basis of protein kinase C isoform function. Physiological reviews 88, 1341–1378, https://doi.org/10.1152/physrev.00034.2007 (2008).
    Sauliere, A. et al. Deciphering biased-agonism complexity reveals a new active AT1 receptor entity. Nature chemical biology 8, 622–630, https://doi.org/10.1038/nchembio.961 (2012).
    Santos, G. A. et al. Comparative analyses of downstream signal transduction targets modulated after activation of the AT1 receptor by two beta-arrestin-biased agonists. Frontiers in pharmacology 6, 131, https://doi.org/10.3389/fphar.2015.00131 (2015).
    Charest, P. G., Terrillon, S. & Bouvier, M. Monitoring agonist-promoted conformational changes of beta-arrestin in living cells by intramolecular BRET. EMBO reports 6, 334–340, https://doi.org/10.1038/sj.embor.7400373 (2005).
    Zimmerman, B. et al. Differential beta-arrestin-dependent conformational signaling and cellular responses revealed by angiotensin analogs. Science signaling 5, ra33, https://doi.org/10.1126/scisignal.2002522 (2012).
    Wisler, J. W. et al. A unique mechanism of beta-blocker action: carvedilol stimulates beta-arrestin signaling. Proceedings of the National Academy of Sciences of the United States of America 104, 16657–16662, https://doi.org/10.1073/pnas.0707936104 (2007).
    Noor, N., Patel, C. B. & Rockman, H. A. Beta-arrestin: a signaling molecule and potential therapeutic target for heart failure. Journal of molecular and cellular cardiology 51, 534–541, https://doi.org/10.1016/j.yjmcc.2010.11.005 (2011).
    Boerrigter, G. et al. Cardiorenal actions of TRV120027, a novel ss-arrestin-biased ligand at the angiotensin II type I receptor, in healthy and heart failure canines: a novel therapeutic strategy for acute heart failure. Circulation. Heart failure 4, 770–778, https://doi.org/10.1161/CIRCHEARTFAILURE.111.962571 (2011).
    Boerrigter, G., Soergel, D. G., Violin, J. D., Lark, M. W. & Burnett, J. C. Jr. TRV120027, a novel beta-arrestin biased ligand at the angiotensin II type I receptor, unloads the heart and maintains renal function when added to furosemide in experimental heart failure. Circulation. Heart failure 5, 627–634, https://doi.org/10.1161/CIRCHEARTFAILURE.112.969220 (2012).
    Felker, G. M. et al. Heart failure therapeutics on the basis of a biased ligand of the angiotensin-2 type 1 receptor. Rationale and design of the BLAST-AHF study (Biased Ligand of the Angiotensin Receptor Study in Acute Heart Failure). JACC. Heart failure 3, 193–201, https://doi.org/10.1016/j.jchf.2014.09.008 (2015).
    Ryba, D. M. et al. Long-Term Biased beta-Arrestin Signaling Improves Cardiac Structure and Function in Dilated Cardiomyopathy. Circulation 135, 1056–1070, https://doi.org/10.1161/CIRCULATIONAHA.116.024482 (2017).
    Galandrin, S. et al. Cardioprotective Angiotensin-(1-7) Peptide Acts as a Natural-Biased Ligand at the Angiotensin II Type 1 Receptor. Hypertension. https://doi.org/10.1161/HYPERTENSIONAHA.116.08118 (2016).
    Rajagopal, K. et al. Beta-arrestin2-mediated inotropic effects of the angiotensin II type 1A receptor in isolated cardiac myocytes. Proceedings of the National Academy of Sciences of the United States of America 103, 16284–16289, https://doi.org/10.1073/pnas.0607583103 (2006).
    Aplin, M. et al. The angiotensin type 1 receptor activates extracellular signal-regulated kinases 1 and 2 by G protein-dependent and -independent pathways in cardiac myocytes and langendorff-perfused hearts. Basic & clinical pharmacology & toxicology 100, 289–295, https://doi.org/10.1111/j.1742-7843.2007.00063.x (2007).
    Kim, J., Ahn, S., Rajagopal, K. & Lefkowitz, R. J. Independent beta-arrestin2 and Gq/protein kinase Czeta pathways for ERK stimulated by angiotensin type 1A receptors in vascular smooth muscle cells converge on transactivation of the epidermal growth factor receptor. The Journal of biological chemistry 284, 11953–11962, https://doi.org/10.1074/jbc.M808176200 (2009).
    Kim, K. S. et al. beta-Arrestin-biased AT1R stimulation promotes cell survival during acute cardiac injury. American journal of physiology. Heart and circulatory physiology 303, H1001–1010, https://doi.org/10.1152/ajpheart.00475.2012 (2012).
    Meng, W. et al. Autocrine and paracrine function of Angiotensin 1-7 in tissue repair during hypertension. American journal of hypertension 27, 775–782, https://doi.org/10.1093/ajh/hpt270 (2014).
    Golomb, E. et al. Angiotensin II maintains, but does not mediate, isoproterenol-induced cardiac hypertrophy in rats. The American journal of physiology 267, H1496–1506 (1994).
    Santos, R. A. et al. Characterization of a new angiotensin antagonist selective for angiotensin-(1-7): evidence that the actions of angiotensin-(1-7) are mediated by specific angiotensin receptors. Brain research bulletin 35, 293–298 (1994).
    Santos, R. A. et al. Impairment of in vitro and in vivo heart function in angiotensin-(1-7) receptor MAS knockout mice. Hypertension 47, 996–1002, https://doi.org/10.1161/01.HYP.0000215289.51180.5c (2006).
    Peiro, C. et al. Endothelial dysfunction through genetic deletion or inhibition of the G protein-coupled receptor Mas: a new target to improve endothelial function. Journal of hypertension 25, 2421–2425, https://doi.org/10.1097/HJH.0b013e3282f0143c (2007).
    Rabelo, L. A. et al. Ablation of angiotensin (1-7) receptor Mas in C57Bl/6 mice causes endothelial dysfunction. Journal of the American Society of Hypertension: JASH 2, 418–424, https://doi.org/10.1016/j.jash.2008.05.003 (2008).
    Gava, E. et al. Angiotensin-(1-7) receptor Mas is an essential modulator of extracellular matrix protein expression in the heart. Regulatory peptides 175, 30–42, https://doi.org/10.1016/j.regpep.2012.01.001 (2012).
    Lautner, R. Q. et al. Discovery and characterization of alamandine: a novel component of the renin-angiotensin system. Circulation research 112, 1104–1111, https://doi.org/10.1161/CIRCRESAHA.113.301077 (2013).
    Ferreira, A. J. et al. The nonpeptide angiotensin-(1-7) receptor Mas agonist AVE-0991 attenuates heart failure induced by myocardial infarction. American journal of physiology. Heart and circulatory physiology 292, H1113–1119, https://doi.org/10.1152/ajpheart.00828.2006 (2007).
    Ebermann, L. et al. The angiotensin-(1-7) receptor agonist AVE0991 is cardioprotective in diabetic rats. European journal of pharmacology 590, 276–280, https://doi.org/10.1016/j.ejphar.2008.05.024 (2008).
    Savergnini, S. Q. et al. Vascular relaxation, antihypertensive effect, and cardioprotection of a novel peptide agonist of the MAS receptor. Hypertension 56, 112–120, https://doi.org/10.1161/HYPERTENSIONAHA.110.152942 (2010).
    Cerbai, E. et al. Long-term treatment of spontaneously hypertensive rats with losartan and electrophysiological remodeling of cardiac myocytes. Cardiovascular research 45, 388–396 (2000).
    Ito, N. et al. Renin-angiotensin inhibition reverses advanced cardiac remodeling in aging spontaneously hypertensive rats. American journal of hypertension 20, 792–799, https://doi.org/10.1016/j.amjhyper.2007.02.004 (2007).
    Loot, A. E. et al. Angiotensin-(1-7) attenuates the development of heart failure after myocardial infarction in rats. Circulation 105, 1548–1550 (2002).
    Rehman, A. et al. Angiotensin type 2 receptor agonist compound 21 reduces vascular injury and myocardial fibrosis in stroke-prone spontaneously hypertensive rats. Hypertension 59, 291–299, https://doi.org/10.1161/HYPERTENSIONAHA.111.180158 (2012).
    Singh, K., Sharma, K., Singh, M. & Sharma, P. L. Possible mechanism of the cardio-renal protective effects of AVE-0991, a non-peptide Mas-receptor agonist, in diabetic rats. Journal of the renin-angiotensin-aldosterone system: JRAAS 13, 334–340, https://doi.org/10.1177/1470320311435534 (2012).
    Benter, I. F. et al. Angiotensin-(1-7) blockade attenuates captopril- or hydralazine-induced cardiovascular protection in spontaneously hypertensive rats treated with NG-nitro-L-arginine methyl ester. Journal of cardiovascular pharmacology 57, 559–567, https://doi.org/10.1097/FJC.0b013e31821324b6 (2011).
    Yousif, M. H., Makki, B., El-Hashim, A. Z., Akhtar, S. & Benter, I. F. Chronic treatment with Ang-(1-7) reverses abnormal reactivity in the corpus cavernosum and normalizes diabetes-induced changes in the protein levels of ACE, ACE2, ROCK1, ROCK2 and omega-hydroxylase in a rat model of type 1 diabetes. Journal of diabetes research 2014, 142154, https://doi.org/10.1155/2014/142154 (2014).
    Durand, M. T. et al. Pyridostigmine restores cardiac autonomic balance after small myocardial infarction in mice. PloS one 9, e104476, https://doi.org/10.1371/journal.pone.0104476 (2014).
    Westermeier, F. et al. Novel players in cardioprotection: Insulin like growth factor-1, angiotensin-(1-7) and angiotensin-(1-9). Pharmacological research 101, 41–55, https://doi.org/10.1016/j.phrs.2015.06.018 (2015).
    Sampaio, W. O. et al. Angiotensin-(1-7) through receptor Mas mediates endothelial nitric oxide synthase activation via Akt-dependent pathways. Hypertension 49, 185–192, https://doi.org/10.1161/01.HYP.0000251865.35728.2f (2007).
    Zhao, J. et al. Effects of the angiotensin-(1-7)/Mas/PI3K/Akt/nitric oxide axis and the possible role of atrial natriuretic peptide in an acute atrial tachycardia canine model. Journal of the renin-angiotensin-aldosterone system: JRAAS 16, 1069–1077, https://doi.org/10.1177/1470320314543723 (2015).

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