NDLI: Trypanosoma cruzi trans-sialidase: a potent and specific survival factor for human Schwann cells by means of phosphatidylinositol 3-kinase/Akt signaling.

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Trypanosoma cruzi trans-sialidase: a potent and specific survival factor for human Schwann cells by means of phosphatidylinositol 3-kinase/Akt signaling.

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Trypanosoma cruzi trans-sialidase: a potent and specific survival factor for human Schwann cells by means of phosphatidylinositol 3-kinase/Akt signaling.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Cavenee, W. K. Pereira, M. A. Chuenkova, M. V. Furnari, F. B.
Description	Author Affiliation: Chuenkova MV ( Parasitology Research Center, Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, USA.);
Abstract	Patients infected with Trypanosoma cruzi may remain asymptomatic for decades and show signs of neuroregeneration in the peripheral nervous system (PNS). In the absence of such neuroregeneration, patients may die in part by extensive neuronal destruction in the gastrointestinal tract. Thus, T. cruzi may, despite their invasion of the PNS, directly prevent cell death to keep nerve destruction in check. Indeed, T. cruzi invasion of Schwann cells, their prime target in PNS, suppressed host-cell apoptosis caused by growth-factor deprivation. The trans-sialidase (TS) of T. cruzi and the Cys-rich domain of TS reproduced the antiapoptotic activity of the parasites at doses (> or =3.0 nM) comparable or lower than those of bona fide mammalian growth factors. This effect was blocked by LY294002, an inhibitor of phosphatidylinositol 3-kinase (PI3K). TS also activated Akt, a downstream effector of PI3K. Ectopic expression of TS in an unrelated parasite, Leishmania major, turned those parasites into activators of Akt in Schwann cells. In contrast, the Cys-rich domain of TS did not block apoptosis in Schwann cells overexpressing dominant-negative Akt or constitutively active PTEN, a negative regulator of PI3K/Akt signaling. The results demonstrate that T. cruzi, through its TS, triggers the survival of host Schwann cells via the PI3K/Akt pathway, suggesting a role for PI3K/Akt in the pathogenesis of Chagas' disease.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	17
Volume Number	98
Language	English
Publisher	National Academy of Sciences
Publisher Date	2001-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Glycoproteins Pharmacology Neuraminidase Phosphatidylinositol 3-Kinases Physiology Protein-Serine-Threonine Kinases Proto-Oncogene Proteins Protozoan Proteins Schwann Cells Drug Effects Signal Transduction Trypanosoma Cruzi Enzymology Tumor Suppressor Proteins Animals Apoptosis Cell Survival Cells, Cultured Chagas Disease Chromones Culture Media, Serum-Free Enzyme Activation Enzyme Inhibitors Genetics Leishmania Major Molecular Sequence Data Morpholines PTEN Phosphohydrolase Antagonists & Inhibitors Phosphoric Monoester Hydrolases Phosphorylation Protein Processing, Post-Translational Deficiency Proto-Oncogene Proteins C-akt Recombinant Fusion Proteins Cytology Parasitology Transfection Pathogenicity Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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