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Am J Physiol Heart Circ Physiol 292: H270-H276, 2007. First published August 25, 2006; doi:10.1152/ajpheart.00576.2006
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Upregulation of {gamma}-catenin compensates for the loss of beta-catenin in adult cardiomyocytes

Jibin Zhou,1,* Jiaxiang Qu,1,* Xian Ping Yi,1,3,* Kelly Graber,1 Lu Huber,1 Xuejun Wang,1 A. Martin Gerdes,1 and Faqian Li1,2

1Cardiovascular Research Institute, South Dakota Health Research Foundation, 2Department of Laboratory Medicine and Pathology, University of South Dakota Sanford School of Medicine and Sioux Valley Hospitals and Health System, Sioux Falls, South Dakota; and 3Department of Pathology, Zhongshan University, Fifth Affiliated Hospital, Zhuhai, Guangdong Province, People’s Republic of China

Submitted 2 June 2006 ; accepted in final form 23 August 2006

Recent progresses in signal transduction have revealed that beta-catenin signaling controls embryonic development, tumorigenesis, cell shape, and polarity. The role of this pathway in myocyte shape regulation during cardiac hypertrophy and failure is, however, not clearly defined. Since homozygous knockout of beta-catenin is embryonically lethal, we have deleted beta-catenin genes specifically in the heart of adult mice by crossing loxP-flanked beta-catenin mice with transgenic mice expressing tamoxifen-activated MerCreMer protein (MCM) driven by the {alpha}-myosin heavy chain promoter. Administration of tamoxifen to homozygous loxP-flanked beta-catenin mice positive for MCM induces the deletion of beta-catenin only in cardiomyocytes. Immunolabeling with beta-catenin antibody demonstrates that 90% of cardiomyocytes completely lose their beta-catenin expression but maintain normal rod-shaped morphology. The intercalated disk of cardiomyocytes lacking beta-catenin is morphologically unremarkable with normal distribution of vinculin, N-cadherin, desmoplakin, ZO-1, connexin43, and {alpha}-, {gamma}-, and p120 catenins. The expression level of these proteins, except that of {gamma}-catenin, is also similar in tamoxifen-treated and control mice with both homozygous loxP-flanked beta-catenin genes and the MCM transgene. Western blot analyses reveal that {gamma}-catenin increases in the heart of beta-catenin knockout mice compared with controls. Confocal microscopy also demonstrates that {gamma}-catenin has significantly increased in the intercalated disk of cardiomyocytes lacking beta-catenin. Echocardiographic data indicate that the knockout mice maintain normal ventricular geometry and cardiac function. The results suggest that upregulation of {gamma}-catenin can compensate for the loss of beta-catenin in cardiomyocytes to maintain normal cardiac structure and function.

catenin; heart; intercalated disk; cardiomyocyte; knockout


Address for reprint requests and other correspondence: Faqian Li, Cardiovascular Research Institute, South Dakota Health Research Foundation, 1100 East 21st St., Suite 700, Sioux Falls, SD 57105 (e-mail address: fli{at}usd.edu)




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