MIERCIO E. A. PEREIRA

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Trypanosoma cruzi, the etiological agent of Chagas' disease, expresses a trans-sialidase at highest levels in infective trypomastigotes, where it attaches to the plasma membrane by a glycophosphoinositol linkage. Bound enzyme sheds into the extracellular milieu in a soluble form. Experiments performed in vitro suggest that the trans-sialidase participates(More)
Trypanosoma cruzi expresses a developmentally regulated neuraminidase (TCNA) implicated in parasite invasion of cells. We isolated full-length DNA clones encoding TCNA. Sequence analysis demonstrated an open reading frame coding for a polypeptide of 1,162 amino acids. In the N-terminus there is a cysteine-rich domain containing a stretch of 332 amino acids(More)
Beyond the presence of insulin receptors, little is known of the mechanisms underlying the biological effects of insulin in the placenta. We show that phosphorylation of MAPK and protein kinase B were enhanced 286 +/- 23% and 393 +/- 17% upon insulin stimulation of JAr placental cells. MAPK activation was prevented by pretreatment with PD98059 but was(More)
The human pathogen Trypanosoma cruzi (Y strain) contains a neuraminidase activity that varies widely in the different developmental stages of the parasite. The specific neuraminidase activity of infective trypomastigotes obtained from tissue culture and from the bloodstream of infected mice is 7 to 15 times higher than that of the acellular culture forms.(More)
T. cruzi invades mammalian cells in various organs after migrating through the ECM. These activities appear to be mediated by a unique 60 kd protein exposed on the T. cruzi surface, which promotes selective adhesion of trypomastigotes to three ECM components: heparin, heparan sulfate, and collagen. The affinity-purified protein binds to host fibroblasts in(More)
Despite the neuronal degeneration in the chronic stage of Chagas' disease, neuron counts actually increase in the preceding, asymptomatic stage, in contrast to the age-related decrease in neuron counts in age-matched normal individuals. Relevant to this observation, we found that the trans-sialidase (TS) of Trypanosoma cruzi, the etiologic agent of Chagas'(More)
Trypanosoma cruzi invades most nucleated mammalian cells by as yet unknown mechanisms. We report here that while T. cruzi attaches to epithelial cells lacking signaling transforming growth factor beta (TGF beta) receptor I or II, the adherent parasites cannot penetrate and replicate inside the mutant cells, as they do in parental cells. Invasion of the(More)
The trans-sialidase (TS) of Trypanosoma cruzi induces survival and differentiation of neuronal and glial cells. This mechanism underlying survival is via phosphatidylinositol 3-kinase (PI3K) but how TS promotes neuronal differentiation remained to be determined. Here we show that TS-induced neurite outgrowth in PC12 cells is through sustained activation of(More)
The neuraminidase/trans-sialidase of Trypanosoma cruzi, the agent of Chagas' disease, promotes differentiation and survival of growth factor-deprived neuronal and glial cells. To gain further insights into the possible neuroprotection of this parasite-derived counterpart of neurotrophic factors (PDNF), we sought to determine whether it mimics growth factors(More)
The transcription factor nuclear factor-kappaB (NF-kappaB) is central to the innate and acquired immune response to microbial pathogens, coordinating cellular responses to the presence of infection. Here we demonstrate a direct role for NF-kappaB activation in controlling intracellular infection in nonimmune cells. Trypanosoma cruzi is an intracellular(More)