Regulation of host cell cyclin D1 by Trypanosoma cruzi in myoblasts

Infection with the parasite Trypanosoma cruzi causes Chagas disease. In this study we demonstrated that there was an increase in cyclin D1 expression in T. cruzi (Tulahuen strain)-infected myoblasts. To examine a possible mechanism for the increased cyclin D1 expression we transfected L6E9 myoblasts...

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Bibliographic Details
Published in:Cell cycle (Georgetown, Tex.) Tex.), 2008-02, Vol.7 (4), p.500-503
Main Authors: Bouzahzah, Boumediene, Yurchenko, Vyacheslav, Nagajyothi, Fnu, Hulit, James, Sadofsky, Moshe, Braunstein, Vicki L., Mukherjee, Shankar, Weiss, Hannah, Machado, Fabiana S., Pestell, Richard G., Lisanti, Michael P., Tanowitz, Herbert B., Albanese, Chris
Format: Article
Language:English
Subjects:
Animals
Binding
Biology
Bioscience
Calcium
Cancer
Cell
Chagas Disease - metabolism
Cycle
Cyclin D1 - genetics
Cyclin D1 - metabolism
DNA Primers - genetics
Gene Expression Regulation
Humans
Landes
Luciferases
Myoblasts - metabolism
Myoblasts - parasitology
Organogenesis
Proteins
Trypanosoma cruzi - metabolism
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Summary:Infection with the parasite Trypanosoma cruzi causes Chagas disease. In this study we demonstrated that there was an increase in cyclin D1 expression in T. cruzi (Tulahuen strain)-infected myoblasts. To examine a possible mechanism for the increased cyclin D1 expression we transfected L6E9 myoblasts with cyclin D1 luciferase reporter constructs and infected with T. cruzi. There was no evidence of an increase in promoter activity. Additionally, quantitative PCR did not demonstrate any change in cyclin D1 message during infection. Moreover, we demonstrated that the cyclin D1 protein was significantly stabilized after infection. Collectively, these data indicate that infection with T. cruzi increases cyclin D1 protein abundance post-translationally.
ISSN:1538-4101
1551-4005
DOI:10.4161/cc.7.4.5327