| First Author | Huang X | Year | 2019 |
| Journal | Gene | Volume | 697 |
| Pages | 40-47 | PubMed ID | 30794912 |
| Mgi Jnum | J:295513 | Mgi Id | MGI:6453905 |
| Doi | 10.1016/j.gene.2019.02.023 | Citation | Huang X, et al. (2019) Knockout of Wdr1 results in cardiac hypertrophy and impaired cardiac function in adult mouse heart. Gene 697:40-47 |
| abstractText | WDR1 is a major cofactor of the actin depolymerizing factor (ADF)/cofilin, accelerating ADF/cofilin-mediated actin disassembly. We had previously showed that WDR1-mediated actin dynamics is required for postnatal myocardial growth and adult myocardial maintenance in mice, in which the detailed phenotypes of adult cardiomyocyte-specific Wdr1 deletion mice had not been analyzed. In this study, we systematically analyzed the role of Wdr1 in adult mouse heart. Adult cardiomyocyte-specific Wdr1 deletion mice (cKO) exhibited cardiac hypertrophy and myocardial fibrosis. Echocardiographic study and electrocardiography revealed impaired contractile function, prolonged QT interval and Tpeak-Tend interval, and abnormal T-wave amplitude in cKO mice. Increased levels of sarcomeric proteins, adherens junction proteins and cofilin, and severe actin filament (F-actin) accumulations were observed in cKO mice heart. Taken together, this finding demonstrates that WDR1 is a critical factor for normal structure and function of adult mouse heart. |
