| First Author | Fujimura L | Year | 2004 |
| Journal | Cardiovasc Res | Volume | 64 |
| Issue | 2 | Pages | 315-21 |
| PubMed ID | 15485691 | Mgi Jnum | J:162743 |
| Mgi Id | MGI:4819697 | Doi | 10.1016/j.cardiores.2004.07.009 |
| Citation | Fujimura L, et al. (2004) Protective role of Nd1 in doxorubicin-induced cardiotoxicity. Cardiovasc Res 64(2):315-21 |
| abstractText | 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. |
