<I>TRYPANOSOMA CRUZI </I>MODULA A VIA ENDOCITICA DE CARDIOMIOCITOS IN VITRO





TRYPANOSOMA CRUZI MODULA A VIA ENDOCITICA DE CARDIOMIOCITOS IN VITRO

(especial para SIIC © Derechos reservados)
Células cardíacas infectadas pelo Trypanosoma cruzi apresentam perda de atividade endocítica possivelmente associada á regulação negativa de GTPases, tais como Rab7 e Rab11 (compartimentos endocíticos tardios e de reciclagem, respectivamente), e de moléculas efetoras como a EEA1, relacionada à Rab5a (envolvida no transporte entre compartimentos endocíticos iniciais).
Autor:
Maria De Nazaré Correia Soeiro
Columnista Experto de SIIC

Institución:
Fundação Oswaldo Cruz


Artículos publicados por Maria De Nazaré Correia Soeiro
Coautores
CF Silva* RA Mota* Maria de Nazaré Correia Soeiro** 
Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brasil*
Fundação Oswaldo Cruz, Rio de Janeiro, Brasil**
Aprobación
5 de Octubre, 2006
Primera edición
19 de Febrero, 2007
Segunda edición, ampliada y corregida
7 de Junio, 2021

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Extensión:  +/-4.83 páginas impresas en papel A4
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Clasificación en siicsalud
Artículos originales > Expertos de Iberoamérica >
página   www.siicsalud.com/des/expertocompleto.php/

Especialidades
Principal: Bioquímica, Infectología
Relacionadas: Cardiología, Diagnóstico por Laboratorio



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Enviar correspondencia a:
MNC Soeiro, Departamento Ultra-Estructura e Biologia Celular, Instituto Oswaldo Cruz, FIOCRUZ, 21045-900, Avenida Brasil 4365, Manguinhos, Rio de Janeiro, Brasil
Bibliografía del artículo
1. Mousavi SA, Malerod L, Berg T, Kjeken R. Clathrin-dependent endocytosis. Biochem J 2004; 377(Pt 1):1-16.
2. Rabinovitch M. Professional and non-professional phagocytes: an introduction. Trends Cell Biol 1995; 5(3):85-87.
3. Soeiro MNC, Mota RA, Batista DGJ, Meirelles MNL. Endocytic pathway in mouse cardiac cells. Cell Struct Funct 2002; 27(6):469-478.
4. Hespanhol RC, Soeiro MNC, Meuser MB, Meirelles MNL, Corte-Real S. The expression of mannose receptors in skin fibroblast and their involvement in Leishmania (L.) amazonensis invasion. J Histochem Cytochem 2005; 53(1):35-44.
5. Marsh M, McMahon HT. The structural era of endocytosis. Science. 1999; 285(5425):215-220.
6. Conner SD, Schmid SL. Regulated portals of entry into the cell. Nature 2003; 422(6927):37-44.
7. Maxfield FR, McGraw TE. Endocytic recycling. Nat Rev Mol Cell Biol 2004; 5(2):121-132.
8. Johannes L, Lamaze C. Clathrin-dependent or not: is it still the question? Traffic 2002; 3(7):443-451.
9. Rabinowitz S, Horstmann H, Gordon S, Griffiths G. Immunocytochemical characterization of the endocytic and phagolysosomal compartments in peritoneal macrophages. J Cell Biol 1992; 116(1):95-112.
10. Desjardins M, Huber LA, Parton RG, Griffiths G. Biogenesis of phagolysosomes proceeds through a sequential series of interactions with the endocytic apparatus. J Cell Biol 1994; 124(5):677-688.
11. Clague MJ. Molecular aspects of the endocytic pathway. Biochem J. 1998; 336 (Pt 2):271-282.
12. Van Vliet C, Thomas EC, Merino-Trigo A, Teasdale RD, Gleeson PA. Intracellular sorting and transport of proteins. Prog Biophys Mol Biol 2003; 83(1):1-45.
13. Miaczynska M, Zerial M. Mosaic organization of the endocytic pathway. Exp Cell Res 2002; 272(1):8-14.
14. Gruenberg J. The endocytic pathway: a mosaic of domains. Nat Rev Mol Cell Biol 2001; 2(10):721-730.
15. Zerial M, McBride H. Rab proteins as membrane organizersNat Rev Mol Cell Biol 2001; 2(2):107-117.
16. Haas A. Reprogramming the phagocytic pathway--intracellular pathogens and their vacuoles. Mol Membr Biol 1998; 15(3):103-121.
17. Hashim S, Mukherjee K, Raje M, Basu SK, Mukhopadhyay A. Live Salmonella modulate expression of Rab proteins to persist in a specialized compartment and escape transport to lysosomes. J Biol Chem 2000; 275(21):16281-16288.
18. Luhrmann A, Streker K, Schuttfort A, Daniels JJ, Haas A. Afipia felis induces uptake by macrophages directly into a nonendocytic compartment. Proc Natl Acad Sci USA 2001; 98(13):7271-7276.
19. Stein MP, Dong J, Wandinger-Ness A. Rab proteins and endocytic trafficking: potential targets for therapeutic intervention. Adv Drug Deliv Rev 2003; 55(11):1421-1437.
20. Walburger A, Koul A, Ferrari G, Nguyen L, Prescianotto-Baschong C, Huygen K, Klebl B, Thompson C, Bacher G, Pieters J. Protein kinase G from pathogenic mycobacteria promotes survival within macrophages. Science 2004; 304(5678):1800-1804.
21. Soeiro MNC, Costa e Silva Filho F, Meirelles MNL. Alterations in the surface charge of heart muscle cells during interaction with Trypanosoma cruzi. Cell Biophys 1995; 26(1):21-44.
22. Soeiro MNC, Paiva MM, Barbosa HS, Meirelles MNL, Araújo-Jorge TC. A cardiomyocyte mannose receptor system is involved in Trypanosoma cruzi invasion and is down-modulated after infection. Cell Struct Funct 1999; 24(3):139-149.
23. Bucci C, Thomsen P, Nicoziani P, McCarthy J, Van Deurs B. Rab7: a key to lysosome biogenesis. Mol Biol Cell 2000; 11(2):467-480.
24. Maxfield FR, McGraw TE. Endocytic recycling. Nat Rev Mol Cell Biol 2004; 5(2):121-132.
25. Soeiro MN, Mota RA, Batista DG, Pereira MC, Meirelles MN. Trypanosoma cruzi infection impairs the endocytosis of zymosan A by cardiomyocytes. Pathobiology 2002; 70(2):69-75.
26. Balligand JL, Ungureanu-Longrois D, Simmons WW, Pimental D, Malinskin TA, Kapturczakn M, Tahan Z, Lowensteinll CJ, Davidoff AJ, Kelly RA, Smith TW, Michel T. Cytokine-inducible nitric oxide synthase (iNOS) expression in cardiac myocytes. Characterization and regulation of iNOS expression and detection of iNOS activity in single cardiac myocytes in vitro. J Biol Chem 1994; 269(44):27580-27588.
27. Machado FS, Martins GA, Aliberti JC, Mestriner FL, Cunha FQ, Silva JS. Trypanosoma cruzi-infected cardiomyocytes produce chemokines and cytokines that trigger potent nitric oxide-dependent trypanocidal activity. Circulation 2000; 102(24):3003-3008.
28. Fichera LE, Albareda MC, Laucella SA, Postan M. Intracellular growth of Trypanosoma cruzi in cardiac myocytes is inhibited by cytokine-induced nitric oxide. release. Infect Immun 2004; 72(1):359-363.
29. Finkel MS, Oddis CV, Jacob TD, Watkins SC, Hattler BG, Simmons RL. Negative inotropic effects of cytokines on the heart mediated by nitric oxide. Science 1992; 257(5068):387-389.
30. Cabeza Meckert PM, Chambo JG, Laguens RP. Presence of cells producing antiheart autoantibodies in the inflammatory infiltrate of chronic chagasic myocarditis. Clin Immunol Immunopathol 1991; 60(1):137-144.
31. Alvarez Domínguez C, Stahl PD. Interferon-gamma selectively induces Rab5a synthesis and processing in mononuclear cells. J Biol Chem 1998; 273(51):33901-33904.
32. Hackstadt T. Redirection of host vesicle trafficking pathways by intracellular parasites. Traffic 2000; 1(2):93-99.
33. Seabra MC, Mules EH, Hume AN. Rab GTPases, intracellular traffic and disease. Trends Mol Med 2002; 8(1):23-30.
34. Chua J, Vergne I, Master S, Deretic V. A tale of two lipids: Mycobacterium tuberculosis phagosome maturation arrest. Curr Opin Microbiol 2004; 7(1):71-77.
35. Sibley LD, Andrews NW. Cell invasion by un-palatable parasites. Traffic 2000; 1(2):100-106.
36. Desjardins M, Descoteaux A. Inhibition of phagolysosomal biogenesis by the Leishmania lipophosphoglycan. J Exp Med 1997; 185(12):2061-2068.
37. Borges VM, Vannier-Santos MA, de Souza W. Subverted transferrin trafficking in Leishmania-infected macrophages. Parasitol Res 1998; 84(10):811-822.
38. Alvarez Domínguez C, Roberts R, Stahl PD. Internalized Listeria monocytogenes modulates intracellular trafficking and delays maturation of the phagosome. J Cell Sci 1997; 110:731-743.

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