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Cardiovascular Research 2004 64(2):315-321; doi:10.1016/j.cardiores.2004.07.009
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Protective role of Nd1 in doxorubicin-induced cardiotoxicity

Lisa Fujimura, Yuji Matsudo, Myengmo Kang, Yasuyuki Takamori, Takeshi Tokuhisa and Masahiko Hatano*

Department of Developmental Genetics (H2), Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba City, Japan

* Corresponding author. Tel.: +81 43 226 2182; fax: +81 43 226 2183. Email address: hatanom{at}faculty.chiba-u.jp

Objective: The Ndl gene, which encodes a novel kelch family protein, is expressed ubiquitously in mouse tissues. In vitro studies suggest that Ndl protein, which binds to actin filaments, functions as a cytoskeletal stabilizer. In order to elucidate a physiological function of Ndl in vivo, we generated Nd1-deficient (Ndl-/-) mice.

Methods: We developed Nd1-/- mice by standard gene targeting technique. Cardiac function was studied in wild type and Nd1-/- mice.

Results: Nd1-/- mice were viable and no gross anatomical abnormality was observed after birth. When mouse embryonic fibroblasts were cultured in the presence of cytochalasin D or doxorubicin, the number of apoptotic cells in the Nd1-/- cell culture was larger that that in the wild-type cell culture. Furthermore, Nd1-/- mice were sensitive to doxorubicin-induced cardiotoxicity with increased numbers of cardiomyocytes apoptosis.

Conclusions: Although Nd1 is dispensable for normal mice development, Nd1 plays a protective role in doxorubicin-induced cardiotoxic responses.

KEYWORDS Actin-binding protein; Doxorubicin; Kelch family protein; Nd1-deficient mice

Time for primary review 38 days


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