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INCREASED ANGIOGENESIS PARALLELS CARDIAC TISSUE REMODELLING IN EXPERIMENTAL ACUTE TRYPANOSOMA CRUZI INFECTION
Remodelação do tecido cardíaco
Doença de Chagas aguda experimental
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Abstract
BACKGROUND Angiogenesis has been implicated in tissue injury in several noninfectious diseases, but its role in Chagas disease
(CD) physiopathology is unclear.
OBJECTIVES The present study aimed to investigate the effect of Trypanosoma cruzi infection on cardiac angiogenesis during the
acute phase of experimental CD.
METHODS The signalling pathway involved in blood vessel formation and cardiac remodelling was evaluated in Swiss Webster
mice infected with the Y strain of T. cruzi. The levels of molecules involved in the regulation of angiogenesis, such as vascular
endothelial growth factor-A (VEGF-A), Flk-1, phosphorylated extracellular-signal-regulated protein kinase (pERK), hypoxiainducible
factor-1α (HIF-1α), CD31, α-smooth muscle actin (α-SMA) and also the blood vessel growth were analysed during T.
cruzi infection. Hearts were analysed using conventional histopathology, immunohistochemistry and western blotting.
FINDINGS In this study, our data demonstrate that T. cruzi acute infection in mice induces exacerbated angiogenesis in the heart
and parallels cardiac remodelling. In comparison with noninfected controls, the cardiac tissue of T. cruzi-infected mice presented
higher levels of (i) HIF-1α, VEGF-A, Flk-1 and pERK; (ii) angiogenesis; (iii) α-SMA+ cells in the tissue; and (iv) collagen -1
deposition around blood vessels and infiltrating throughout the myocardium.
MAIN CONCLUSIONS We observed cardiac angiogenesis during acute experimental T. cruzi infection parallels cardiac
inflammation and remodelling.
Keywords in Portuguese
Angiogênese cardíacaRemodelação do tecido cardíaco
Doença de Chagas aguda experimental
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