Disarray of sarcomeric alpha-actinin in cardiomyocytes infected by Trypanosoma cruzi

dc.creatorMelo, T. G.
dc.creatorAlmeida, D. S.
dc.creatorMeirelles, M. N. S. L.
dc.creatorPereira, M. C. S.
dc.date2020-01-28T18:10:35Z
dc.date2020-01-28T18:10:35Z
dc.date2006
dc.date.accessioned2023-09-27T00:04:20Z
dc.date.available2023-09-27T00:04:20Z
dc.identifierMELO, T. G. et al. Disarray of sarcomeric alpha-actinin in cardiomyocytes infected by Trypanosoma cruzi. Parasitology, v. 133, p. 171-178, 2006.
dc.identifier0031-1820
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/39566
dc.identifier10.1017/S0031182006000011
dc.identifier1469-8161
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8897138
dc.descriptionInfection with Trypanosoma cruzi causes acute myocarditis and chronic cardiomyopathy. Remarkable changes have been demonstrated in the structure and physiology of cardiomyocytes during infection by this parasite that may contribute to the cardiac dysfunction observed in Chagas’ disease. We have investigated the expression ofa-actinin, an actin-binding protein that plays a key role in the formation and maintenance of Z-lines, during the T. cruzi-cardiomyocyte interaction in vitro. Immunolocalization of a-actinin in control cardiomyocytes demonstrated a typical periodicity in the Z line of cardiac myofibrils, as well as its distribution at focal adhesion sites and along the cell–cell junctions. No significant changes were observed in the localization ofa-actinin after 24 h of infection. In contrast, depletion of sarcomeric distribution ofa-actinin occurred after 72 h in T. cruzi-infected cardiomyocytes, while no change occurred at focal adhesion contacts. Biochemical assays demonstrated a reduction of 46% and 32% in the expression of a-actinin after 24 h and 72 h of infection, respectively. Intracellular parasites were also stained with an anti-a-actinin antibody that recognized a protein of 78 kDa by Western blot. Taken together, our data demonstrate a degeneration of the myofibrils in cardiomyocytes induced by T. cruzi infection, rather than a disassembly of the I bands within sarcomeres.
dc.description2025-01-01
dc.formatapplication/pdf
dc.languageeng
dc.publisherCambridge University Press
dc.rightsrestricted access
dc.subjectTrypanosoma cruzi
dc.subjectCardiomiócito
dc.subjectAlfa-actinina
dc.subjectAdesão focal
dc.subjectCardiomyocyte
dc.subjectTrypanosoma cruzi
dc.subjectAlpha-actinin
dc.subjectFocal adhesion
dc.subjectZ-lines
dc.titleDisarray of sarcomeric alpha-actinin in cardiomyocytes infected by Trypanosoma cruzi
dc.typeArticle


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