Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/8986
Title: Gap junctions and chagas disease
Authors: Adesse, Daniel Pedra
Goldenberg, Regina Coeli dos Santos
Fortes, Fabio da Silva de Azevedo
Jasmin
Iacobas, Dumitru Andrei
Iacobas, Sanda
Carvalho, Antonio Carlos Campos de
Meirelles, Maria de Nazareth Leal de
Huang, Huan
Soares, Milena Botelho Pereira
Tanowitz, Herbert Bernard
Garzoni, Luciana Ribeiro
Spray, David Conover
Affilliation: Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil
Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil
Centro Universitario Stadual da Zona Oeste. Colegiado de Ciencias Biologicas e da Saude (CCBS). Rio de Janeiro, RJ, Brasil
Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil / Albert Einstein College of Medicine. Dominick P. Purpura. Department of Neuroscience. Bronx, NEW York, USA
Albert Einstein College of Medicine. Dominick P. Purpura. Department of Neuroscience. Bronx, NEW York, USA
Albert Einstein College of Medicine. Dominick P. Purpura. Department of Neuroscience. Bronx, NEW York, USA
Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil / Albert Einstein College of Medicine. Dominick P. Purpura. Department of Neuroscience. Bronx, NEW York, USA
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil
Albert Einstein College of Medicine. Department of Pathology. Bronx, New York, USA
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Albert Einstein College of Medicine. Department of Pathology. Bronx, New York, USA
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil
Albert Einstein College of Medicine. Dominick P. Purpura. Department of Neuroscience. Bronx, NEW York, USA
Abstract: Gap junction channels provide intercellular communication between cells. In the heart, these channels coordinate impulse propagation along the conduction system and through the contractile musculature, thereby providing synchronous and optimal cardiac output. As in other arrhythmogenic cardiac diseases, chagasic cardiomyopathy is associated with decreased expression of the gap junction protein connexin43 (Cx43) and its gene. Our studies of cardiac myocytes infected with Trypanosoma cruzi have revealed that synchronous contraction is greatly impaired and gap junction immunoreactivity is lost in infected cells. Such changes are not seen for molecules forming tight junctions, another component of the intercalated disc in cardiac myocytes. Transcriptomic studies of hearts from mouse models of Chagas disease and from acutely infected cardiac myocytes in vitro indicate profound remodelling of gene expression patterns involving heart rhythm determinant genes, suggesting underlying mechanisms of the functional pathology. One curious feature of the altered expression of Cx43 and its gene expression is that it is limited in both extent and location, suggesting that the more global deterioration in cardiac function may result in part from spread of damage signals from more seriously compromised cells to healthier ones.
DeCS: Cardiomiopatia Chagásica/parasitologia
Junções Gap/fisiologia
Coração/fisiologia
Coração/parasitologia
Trypanosoma cruzi/patogenicidade
Animais
Células Cultivadas
Perfilação da Expressão Gênica
Interações Hospedeiro-Patógeno
Humanos
Camundongos
Células Musculares/parasitologia
Células Musculares/fisiologia
Issue Date: 2011
Publisher: Elsevier
Citation: ADESSE, D. P. et al. Gap junctions and chagas disease. Advances in Parasitology, v. 76, p. 63-81, 2011.
DOI: 10.1016/B978-0-12-385895-5.00003-7.
ISSN: 0065-308X
Copyright: open access
Appears in Collections:BA - IGM - Artigos de Periódicos

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