Impairment of the Plasmodium falciparum erythrocytic cycle induced by angiotensin peptides

dc.creatorSaraiva, Victor Barbosa
dc.creatorSilva, Leandro de Souza
dc.creatorSilva, Claudio Teixeira Ferreira da
dc.creatorSilva Filho, João Luiz
dc.creatorFerreira, André Teixeira
dc.creatorPerales, Jonas
dc.creatorSouza, Mariana Conceição
dc.creatorHenriques, Maria das Graças
dc.creatorNeves, Celso Caruso-
dc.creatorPinheiro, Ana Acacia de Sá
dc.date2018-03-27T16:52:15Z
dc.date2018-03-27T16:52:15Z
dc.date2011
dc.date.accessioned2023-09-26T20:18:02Z
dc.date.available2023-09-26T20:18:02Z
dc.identifierSARAIVA, Victor Barbosa; et al. Impairment of the Plasmodium falciparum Erythrocytic Cycle Induced by Angiotensin Peptides. Plos One, v.6, n.2, e17174, 9p, Fe. 2011.
dc.identifier1932-6203
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/25528
dc.identifier10.1371/journal.pone.0017174
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8853679
dc.descriptionPlasmodium falciparum causes the most serious complications of malaria and is a public health problem worldwide with over 2 million deaths each year. The erythrocyte invasion mechanisms by Plasmodium sp. have been well described, however the physiological aspects involving host components in this process are still poorly understood. Here, we provide evidence for the role of renin-angiotensin system (RAS) components in reducing erythrocyte invasion by P. falciparum. Angiotensin II (Ang II) reduced erythrocyte invasion in an enriched schizont culture of P. falciparum in a dose-dependent manner. Using mass spectroscopy, we showed that Ang II was metabolized by erythrocytes to Ang IV and Ang-(1-7). Parasite infection decreased Ang-(1-7) and completely abolished Ang IV formation. Similar to Ang II, Ang-(1-7) decreased the level of infection in an A779 (specific antagonist of Ang-(1-7) receptor, MAS)-sensitive manner. 10(-7) M PD123319, an AT(2) receptor antagonist, partially reversed the effects of Ang-(1-7) and Ang II. However, 10(-6) M losartan, an antagonist of the AT(1) receptor, had no effect. Gs protein is a crucial player in the Plasmodium falciparum blood cycle and angiotensin peptides can modulate protein kinase A (PKA) activity; 10(-8) M Ang II or 10(-8) M Ang-(1-7) inhibited this activity in erythrocytes by 60% and this effect was reversed by 10(-7) M A779. 10(-6) M dibutyryl-cAMP increased the level of infection and 10(-7) M PKA inhibitor decreased the level of infection by 30%. These results indicate that the effect of Ang-(1-7) on P. falciparum blood stage involves a MAS-mediated PKA inhibition. Our results indicate a crucial role for Ang II conversion into Ang-(1-7) in controlling the erythrocytic cycle of the malaria parasite, adding new functions to peptides initially described to be involved in the regulation of vascular tonus.
dc.formatapplication/pdf
dc.languageeng
dc.publisherPublic Library of Science
dc.rightsopen access
dc.subjectPlasmodium falciparum
dc.subjectPeptídeos
dc.subjectPeptides da angiotensina
dc.subjectmalaria
dc.subjectCiclo Eritrocítico
dc.subjectPlasmodium falciparum
dc.subjectPlasmodium falciparum
dc.subjectAngiotensin Peptides
dc.subjectErythrocytic Cycle
dc.subjectmalaria
dc.titleImpairment of the Plasmodium falciparum erythrocytic cycle induced by angiotensin peptides
dc.typeArticle


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