Arginase induction promotes Trypanosoma cruzi intracellular replication of Cruzipain-treated J774 cells through the activation of multiple signaling pathways

Given that arginase activation may effectively influence nitric oxide (NO) production in macrophages, we have investigated the intracellular signals that regulate L-arginine metabolism and its influence on Trypanosoma cruzi growth. We demonstrate that cruzipain (Cz), a parasite antigen, induces argi...

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Autor principal: Stempin, C.C
Otros Autores: Tanos, T.B, Coso, O.A, Cerbán, F.M
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 2004
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Acceso en línea:Registro en Scopus
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100 1 |a Stempin, C.C. 
245 1 0 |a Arginase induction promotes Trypanosoma cruzi intracellular replication of Cruzipain-treated J774 cells through the activation of multiple signaling pathways 
260 |c 2004 
270 1 0 |m Cerban, F.M.; Departamento de Bioquimica Clinica, Facultad de Ciencias Quimicas, Universidad Nacional de Cordoba, Haya de la Torre Medina Allende s/n, 5000 Cordoba, Argentina; email: fcerban@bioclin.fcq.unc.edu.ar 
506 |2 openaire  |e Política editorial 
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520 3 |a Given that arginase activation may effectively influence nitric oxide (NO) production in macrophages, we have investigated the intracellular signals that regulate L-arginine metabolism and its influence on Trypanosoma cruzi growth. We demonstrate that cruzipain (Cz), a parasite antigen, induces arginase I expression in J774 cells, and the pretreatment of Cz-treated cells with N-omega-hydroxy-L-arginine (arginase inhibitor) leads to a dramatic decrease in amastigote growth. The study of intracellular signals shows that genistein [tyrosine kinase (TK) inhibitor], KT5720 [protein kinase (PK) A inhibitor] and SB203580 [p38 mitogen-activated protein kinase (MAPK) inhibitor] significantly decrease Cz-induced arginase activation. However, calphostin C (PKC inhibitor) and PD98059 [p44/p42 MAPK kinase (MEK) inhibitor] did not cause a significant change. To determine if signaling pathways triggered by Cz were involved in the T. cruzi growth, we studied the effect of those inhibitors. In Cz-treated cells- pre-incubated with TK, PKA or p38 MAPK inhibitors - the balance of NO/urea was biased towards NO, and the amastigote growth was diminished. Besides, genistein and mainly KT5720 induced down-regulation of arginase I expression in Cz-treated cells. Thus, activation of TK, PKA and p38 MAPK by Cz induces an increase of arginase activity in macrophages and the subsequent T. cruzi growth.  |l eng 
593 |a Departamento de Bioquimica Clinica, Facultad de Ciencias Quimicas, Universidad Nacional de Cordoba, Haya de la Torre Medina Allende s/n, 5000 Cordoba, Argentina 
593 |a Dept. de Fisiol. Biol. Molec. y Cel., Fac. de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina 
690 1 0 |a ARGINASE 
690 1 0 |a MACROPHAGE 
690 1 0 |a PARASITE ANTIGEN 
690 1 0 |a PROTEIN KINASE 
690 1 0 |a TRYPANOSOMA CRUZI 
690 1 0 |a 2 (2 AMINO 3 METHOXYPHENYL)CHROMONE 
690 1 0 |a 4 (4 FLUOROPHENYL) 2 (4 METHYLSULFINYLPHENYL) 5 (4 PYRIDYL)IMIDAZOLE 
690 1 0 |a ARGINASE 
690 1 0 |a ARGININE 
690 1 0 |a CALPHOSTIN C 
690 1 0 |a CARBAZOLE DERIVATIVE 
690 1 0 |a CRUZIPAIN 
690 1 0 |a CYCLIC AMP DEPENDENT PROTEIN KINASE 
690 1 0 |a CYCLIC AMP DEPENDENT PROTEIN KINASE INHIBITOR 
690 1 0 |a CYSTEINE PROTEINASE 
690 1 0 |a DRUG DERIVATIVE 
690 1 0 |a GENISTEIN 
690 1 0 |a GROWTH INHIBITOR 
690 1 0 |a IMIDAZOLE DERIVATIVE 
690 1 0 |a INDOLE DERIVATIVE 
690 1 0 |a KT 5720 
690 1 0 |a MITOGEN ACTIVATED PROTEIN KINASE 
690 1 0 |a MITOGEN ACTIVATED PROTEIN KINASE INHIBITOR 
690 1 0 |a MITOGEN ACTIVATED PROTEIN KINASE P38 
690 1 0 |a N(G) HYDROXYARGININE 
690 1 0 |a N(OMEGA) HYDROXYARGININE 
690 1 0 |a N(OMEGA)-HYDROXYARGININE 
690 1 0 |a NITRIC OXIDE 
690 1 0 |a PARASITE ANTIGEN 
690 1 0 |a PROTEIN KINASE C INHIBITOR 
690 1 0 |a PROTEIN P42 
690 1 0 |a PROTEIN P44 
690 1 0 |a PROTEIN TYROSINE KINASE 
690 1 0 |a PROTEIN TYROSINE KINASE INHIBITOR 
690 1 0 |a PYRIDINE DERIVATIVE 
690 1 0 |a PYRROLE DERIVATIVE 
690 1 0 |a UNCLASSIFIED DRUG 
690 1 0 |a UREA 
690 1 0 |a AMASTIGOTE 
690 1 0 |a AMINO ACID METABOLISM 
690 1 0 |a ANIMAL 
690 1 0 |a ANIMAL CELL 
690 1 0 |a ARTICLE 
690 1 0 |a BIOSYNTHESIS 
690 1 0 |a CELL DIVISION 
690 1 0 |a CELL LINE 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a DEVELOPMENTAL STAGE 
690 1 0 |a DOWN REGULATION 
690 1 0 |a DRUG EFFECT 
690 1 0 |a ENZYME ACTIVATION 
690 1 0 |a ENZYME INDUCTION 
690 1 0 |a ENZYME INHIBITION 
690 1 0 |a ENZYMOLOGY 
690 1 0 |a GROWTH, DEVELOPMENT AND AGING 
690 1 0 |a INCUBATION TIME 
690 1 0 |a MACROPHAGE 
690 1 0 |a METABOLISM 
690 1 0 |a MOUSE 
690 1 0 |a NONHUMAN 
690 1 0 |a PHYSIOLOGY 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a PROTEIN EXPRESSION 
690 1 0 |a SIGNAL TRANSDUCTION 
690 1 0 |a TRYPANOSOMA CRUZI 
690 1 0 |a ANIMALS 
690 1 0 |a ARGINASE 
690 1 0 |a ARGININE 
690 1 0 |a CARBAZOLES 
690 1 0 |a CELL DIVISION 
690 1 0 |a CYCLIC AMP-DEPENDENT PROTEIN KINASES 
690 1 0 |a CYSTEINE ENDOPEPTIDASES 
690 1 0 |a ENZYME INDUCTION 
690 1 0 |a GENISTEIN 
690 1 0 |a GROWTH INHIBITORS 
690 1 0 |a IMIDAZOLES 
690 1 0 |a MITOGEN-ACTIVATED PROTEIN KINASES 
690 1 0 |a P38 MITOGEN-ACTIVATED PROTEIN KINASES 
690 1 0 |a PROTEIN-TYROSINE KINASES 
690 1 0 |a PYRIDINES 
690 1 0 |a PYRROLES 
690 1 0 |a SIGNAL TRANSDUCTION 
690 1 0 |a TRYPANOSOMA CRUZI 
650 1 7 |2 spines  |a INDOLES 
700 1 |a Tanos, T.B. 
700 1 |a Coso, O.A. 
700 1 |a Cerbán, F.M. 
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