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dc.contributor.authorMukherjee, S
dc.contributor.authorSadekar, N
dc.contributor.authorAshton, A
dc.contributor.authorHuang, H
dc.contributor.authorSpray, D
dc.contributor.authorLisanti, Michael P
dc.contributor.authorMachado, F
dc.contributor.authorWeiss, L
dc.contributor.authorTanowitz, H
dc.date.accessioned2013-05-20T12:47:17Z
dc.date.available2013-05-20T12:47:17Z
dc.date.issued2013-04
dc.identifier.citationIdentification of a functional prostanoid-like receptor in the protozoan parasite, trypanosoma cruzi. 2013, 112 (4):1417-25 Parasitol Resen_GB
dc.identifier.issn1432-1955
dc.identifier.pmid23403991
dc.identifier.doi10.1007/s00436-012-3271-5
dc.identifier.urihttp://hdl.handle.net/10541/292376
dc.description.abstractTrypanosoma cruzi infection in humans and experimental animals causes Chagas disease which is often accompanied by myocarditis, cardiomyopathy, and vasculopathy. T. cruzi-derived thromboxane A2 (TXA2) modulates vasculopathy and other pathophysiological features of Chagasic cardiomyopathy. Here, we provide evidence that epimastigotes, trypomastigotes, and amastigotes of T. cruzi (Brazil and Tulahuen strains) express a biologically active prostanoid receptor (PR) that is responsive to TXA2 mimetics, e.g. IBOP. This putative receptor, TcPR, is mainly localized in the flagellar membrane of the parasites and shows a similar glycosylation pattern to that of bona fide thromboxane prostanoid (TP) receptors obtained from human platelets. Furthermore, TXA2-PR signal transduction activates T. cruzi-specific MAPK pathways. While mammalian TP is a G-protein coupled receptor (GPCR); T. cruzi genome sequencing has not demonstrated any confirmed GPCRs in these parasites. Based on this genome sequencing it is likely that TcPR is unique in these protists with no counterpart in mammals. TXA2 is a potent vasoconstrictor which contributes to the pathogenesis of Chagasic cardiovascular disease. It may, however, also control parasite differentiation and proliferation in the infected host allowing the infection to progress to a chronic state.
dc.language.isoenen
dc.rightsArchived with thanks to Parasitology researchen_GB
dc.titleIdentification of a functional prostanoid-like receptor in the protozoan parasite, trypanosoma cruzi.en
dc.typeArticleen
dc.contributor.departmentDepartment of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY, USA. sankar.mukhopadhyay@einstein.yu.eduen_GB
dc.identifier.journalParasitology Researchen_GB
html.description.abstractTrypanosoma cruzi infection in humans and experimental animals causes Chagas disease which is often accompanied by myocarditis, cardiomyopathy, and vasculopathy. T. cruzi-derived thromboxane A2 (TXA2) modulates vasculopathy and other pathophysiological features of Chagasic cardiomyopathy. Here, we provide evidence that epimastigotes, trypomastigotes, and amastigotes of T. cruzi (Brazil and Tulahuen strains) express a biologically active prostanoid receptor (PR) that is responsive to TXA2 mimetics, e.g. IBOP. This putative receptor, TcPR, is mainly localized in the flagellar membrane of the parasites and shows a similar glycosylation pattern to that of bona fide thromboxane prostanoid (TP) receptors obtained from human platelets. Furthermore, TXA2-PR signal transduction activates T. cruzi-specific MAPK pathways. While mammalian TP is a G-protein coupled receptor (GPCR); T. cruzi genome sequencing has not demonstrated any confirmed GPCRs in these parasites. Based on this genome sequencing it is likely that TcPR is unique in these protists with no counterpart in mammals. TXA2 is a potent vasoconstrictor which contributes to the pathogenesis of Chagasic cardiovascular disease. It may, however, also control parasite differentiation and proliferation in the infected host allowing the infection to progress to a chronic state.


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