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Regulation of host cell cyclin D1 by Trypanosoma cruzi in myoblasts

Boumediene Bouzahzah, Vyacheslav Yurchenko, Fnu Nagajyothi, James Hulit, Moshe Sadofsky, Vicki L. Braunstein, Shankar Mukherjee, Hannah Weiss, Fabiana S. Machado, Richard G. Pestell, Michael P. Lisanti, Herbert B. Tanowitz and Chris Albanese

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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.

Authors

Boumediene Bouzahzah

Albert Einstein College of Medicine; Bronx, NY

Vyacheslav Yurchenko

Albert Einstein College of Medicine; Bronx, NY

Fnu Nagajyothi

Albert Einstein College of Medicine; Bronx, NY

James Hulit

Albert Einstein College of Medicine; Bronx, NY

Moshe Sadofsky

Albert Einstein College of Medicine; Bronx, NY

Vicki L. Braunstein

Albert Einstein College of Medicine; Bronx, NY

Shankar Mukherjee

Albert Einstein College of Medicine; Bronx, NY

Hannah Weiss

Albert Einstein College of Medicine; Bronx, NY

Fabiana S. Machado

University of Cincinnati College of Medicine; Cincinnati, OH

Richard G. Pestell

Kimmel Cancer Center; Philadelphia, PA

Michael P. Lisanti

Thomas Jefferson University; Philadelphia, PA

Herbert B. Tanowitz

Albert Einstein College of Medicine; Bronx, NY

Chris Albanese

Georgetown University Medical Center; Washington DC USA

Purchase article for $19

Subscribe to this journal for $129/year