Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/30921
Title: Heme-induced Trypanosoma cruzi proliferation is mediated by CaM kinase II
Authors: Souza, C. F.
Carneiro, A. B.
Silveira, A. B.
Laranja, G. A. T.
Silva Neto, M. A. C.
Costa, S. C. Gonçalves da
Paes, M. C.
Affilliation: Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunomodulação e Protozoologia. Rio de Janeiro, RJ. Brasil.
Universidade Federal do Rio de Janeiro. Instituto de Bioquímica Médica Leopoldo de Meis. Laboratório de Sinalização Celular. Rio de Janeiro, RJ, Brasil.
Universidade Federal do Rio de Janeiro. Instituto de Bioquímica Médica Leopoldo de Meis. Laboratório de Sinalização Celular. Rio de Janeiro, RJ, Brasil.
Universidade do Estado do Rio de Janeiro. Instituto de Biologia Roberto Alcantara Gomes. Departamento de Bioquímica. Laboratório de Interação Tripanosomatídeos e Vetores. Rio de Janeiro, RJ, Brasil.
Universidade Federal do Rio de Janeiro. Instituto de Bioquímica Médica Leopoldo de Meis. Laboratório de Sinalização Celular. Rio de Janeiro, RJ, Brasil / Instituto Nacional de Ciência e Tecnologia. Entomologia Molecular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunomodulação e Protozoologia. Rio de Janeiro, RJ. Brasil.
Universidade do Estado do Rio de Janeiro. Instituto de Biologia Roberto Alcantara Gomes. Departamento de Bioquímica. Laboratório de Interação Tripanosomatídeos e Vetores. Rio de Janeiro, RJ, Brasil / Instituto Nacional de Ciência e Tecnologia. Entomologia Molecular. Rio de Janeiro, RJ, Brasil.
Abstract: Trypanosoma cruzi, the etiologic agent of Chagas disease, is transmitted through triatomine vectors during their blood-meal on vertebrate hosts. These hematophagous insects usually ingest approximately 10mM of heme bound to hemoglobin in a single meal. Blood forms of the parasite are transformed into epimastigotes in the crop which initiates a few hours after parasite ingestion. In a previous work, we investigated the role of heme in parasite cell proliferation and showed that the addition of heme significantly increased parasite proliferation in a dose-dependent manner [1]. To investigate whether the heme effect is mediated by protein kinase signalling pathways, parasite proliferation was evaluated in the presence of several protein kinase (PK) inhibitors. We found that only KN-93, a classical inhibitor of calcium-calmodulin-dependent kinases (CaMKs), blocked heme-induced cell proliferation. KN-92, an inactive analogue of KN-93, was not able to block this effect. A T. cruzi CaMKII homologue is most likely the main enzyme involved in this process since parasite proliferation was also blocked when Myr-AIP, an inhibitory peptide for mammalian CaMKII, was included in the cell proliferation assay. Moreover, CaMK activity increased in parasite cells with the addition of heme as shown by immunological and biochemical assays. In conclusion, the present results are the first strong indications that CaMKII is involved in the heme-induced cell signalling pathway that mediates parasite proliferation.
Keywords: Heme
Trypanosoma cruzi
Ca2+/calmodulin kinase II
Chagas Disease
keywords: Heme
Trypanosoma cruzi
Doença de Chagas
Issue Date: 2009
Publisher: Elsevier
Citation: SOUZA, C. F. et al. Heme-induced Trypanosoma cruzi proliferation is mediated by CaM kinase II. Biochemical and Biophysical Research Communications, v.390, p.541–546, Oct. 2009.
DOI: 10.1016/j.bbrc.2009.09.135
ISSN: 0006-291X
Copyright: restricted access
Appears in Collections:IOC - Artigos de Periódicos

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