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Originally published as JHC exPRESS on July 11, 2005.
doi:10.1369/jhc.5A6654.2005
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Journal of Histochemistry and Cytochemistry
Volume 54 (6): 605-614, 2006
Copyright ©The Histochemical Society, Inc.

Trypanosoma cruzi Modulates the Expression of Rabs and Alters the Endocytosis in Mouse Cardiomyocytes In Vitro

Denise G.J. Batista1, Cristiane F. Silva, Renata A. Mota, Lilian C. Costa, Maria N.L. Meirelles, Marcelo Meuser-Batista and Maria N.C. Soeiro1

Lab. Biologia Celular (DGJB,CFS,RAM,LCC,MM-B,MNCS), Lab. Ultra-estrutura Celular (MNLM), Departamento Ultra-estrutura e Biologia Celular, Instituto Oswaldo Cruz, FIOCRUZ, Manguinhos, Rio de Janeiro, RJ, Brasil

Correspondence to: M.N.C. Soeiro, Departamento Ultra-estrutura e Biologia Celular, Instituto Oswaldo Cruz, FIOCRUZ, Avenida Brasil 4365, Manguinhos, 21045-900, Rio de Janeiro, RJ, Brasil. E-mail: soeiro{at}ioc.fiocruz.br

Chagas disease is an incurable illness caused by the protozoan Trypanosoma cruzi. Cardiomyocytes represent important targets for the parasite infection and alterations in their physiology were reported. Because endocytosis is involved in different cellular events and guanosine triphosphatase (GTPase) Rab proteins play important roles in various aspects of the membrane traffic, our aim was to characterize the expression of Rab proteins in T. cruzi–infected cardiomyocytes, which displayed a downregulation of Rab7 and Rab11, whereas the expression of Rab5a was maintained in the infected cultures even after longer periods of parasite internalization, but early endosome antigen 1 was partially downregulated. The parasite infection also decreased the uptake of fluid phase ligands by the cardiac cultures. The regulation of GTPase proteins and effector molecules can contribute to the altered physiology of the host cells by modifying the normal incoming of nutrients as well as interfering with other important events related to the endocytic pathway. (J Histochem Cytochem 54:605–614, 2006)

Key Words: cardiomyocytes • Trypanosoma cruzi • endocytosis • GTPases • Rab proteins


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