| First Author | Ramakrishna S | Year | 2007 |
| Journal | Dev Dyn | Volume | 236 |
| Issue | 4 | Pages | 1000-13 |
| PubMed ID | 17366632 | Mgi Jnum | J:119481 |
| Mgi Id | MGI:3702262 | Doi | 10.1002/dvdy.21113 |
| Citation | Ramakrishna S, et al. (2007) Myocardium defects and ventricular hypoplasia in mice homozygous null for the Forkhead Box m1 transcription factor. Dev Dyn 236(4):1000-1013 |
| abstractText | The Forkhead Box m1 (Foxm1) transcription factor is expressed in cardiomyocytes and cardiac endothelial cells during heart development. In this study, we used a novel Foxm1 -/- mouse line to demonstrate that Foxm1-deletion causes ventricular hypoplasia and diminished DNA replication and mitosis in developing cardiomyocytes. Proliferation defects in Foxm1 -/- hearts were associated with a reduced expression of Cdk1-activator Cdc25B phosphatase and NFATc3 transcription factor, and with abnormal nuclear accumulation of the Cdk-inhibitor p21(Cip1) protein. Depletion of Foxm1 levels by siRNA caused altered expression of these genes in cultured HL-1 cardiomyocytes. Endothelial-specific deletion of the Foxm1 fl/fl allele in Tie2-Cre Foxm1 fl/fl embryos did not influence heart development and cardiomyocyte proliferation. Foxm1 protein binds to the -9,259/-9,288-bp region of the endogenous mouse NFATc3 promoter, indicating that Foxm1 is a transcriptional activator of the NFATc3 gene. Foxm1 regulates expression of genes essential for the proliferation of cardiomyocytes during heart development. Developmental Dynamics 236:1000-1013, 2007. (c) 2007 Wiley-Liss, Inc. |
