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Background  Heart anomalies are the most frequently observed among all human congenital defects. As with the situation for neural tube defects (NTDs), it has been demonstrated that women who use multivitamins containing folic acid peri-conceptionally have a reduced risk for delivering offspring with conotruncal heart defects [ 1 - 3 ]. Cellular folate transport is mediated by a receptor or binding protein and by an anionic transporter protein system. Defective function of the  Folr1  (also known as  Folbp1 ; homologue of human  FRα ) gene in mice results in inadequate transport, accumulation, or metabolism of folate during cardiovascular morphogenesis.    Results  We have observed cardiovascular abnormalities including outflow tract and aortic arch arterial defects in genetically compromised  Folr1  knockout mice. In order to investigate the molecular mechanisms underlying the failure to complete development of outflow tract and aortic arch arteries in the  Folr1  knockout mouse model, we examined tissue-specific gene expression difference between  Folr1  nullizygous embryos and morphologically normal heterozygous embryos during early cardiac development (14-somite stage), heart tube looping (28-somite stage), and outflow track septation (38-somite stage). Microarray analysis was performed as a primary screening, followed by investigation using quantitative real-time PCR assays. Gene ontology analysis highlighted the following ontology groups: cell migration, cell motility and localization of cells, structural constituent of cytoskeleton, cell-cell adhesion, oxidoreductase, protein folding and mRNA processing. This study provided preliminary data and suggested potential candidate genes for further description and investigation.    Conclusion  The results suggested that  Folr1  gene ablation and abnormal folate homeostasis altered gene expression in developing heart and conotruncal tissues. These changes affected normal cytoskeleton structures, cell migration and motility as well as cellular redox status, which may contribute to cardiovascular abnormalities in mouse embryos lacking  Folr1  gene activity.

Differentially expressed genes in embryonic cardiac tissues of mice lacking Folr1gene activity