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The Journal of Immunology, 2005, 175: 7981-7988.
Copyright © 2005 by The American Association of Immunologists

Stabilized {beta}-Catenin Extends Thymocyte Survival by Up-Regulating Bcl-xL

Huimin Xie, Zhaofeng Huang, Maureen S. Sadim1 and Zuoming Sun2

Department of Microbiology and Immunology, College of Medicine, University of Illinois, Chicago, IL 60612

CD4+CD8+ double-positive (DP) thymocytes, which are extremely sensitive to apoptosis, specifically up-regulate Bcl-xL to extend their lifespan. Deletion of the Bcl-xL gene leads to premature apoptosis of the thymocytes. In this study, we show that stabilization of {beta}-catenin, a critical coactivator for T cell factor (TCF), enhances DP thymocyte survival via up-regulating Bcl-xL. Spontaneous or glucocorticoid-induced thymocyte apoptosis was associated with reduced levels of {beta}-catenin and Bcl-xL. Transgenic expression of a stabilized {beta}-catenin protected DP thymocytes from both spontaneous and glucocorticoid-induced apoptosis, resulting in significantly increased thymic cellularity. Compared with the wild-type mice, both protein and transcript levels of Bcl-xL were significantly increased in thymocytes of {beta}-catenin transgenic mice. In addition, TCF-1 as well as {beta}-catenin were able to stimulate transcriptional activity of the reporter driven by a Bcl-xL promoter. {beta}-Catenin/TCF is thus able to act as a signal to up-regulate Bcl-xL levels in DP thymocytes, resulting in their enhanced survival.




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