Table 3.
Hif‐1α cKO and O2 Deprivation Cause Cardiac Defects
| Defect | Wnt1Cre | β‐actinCre Early | β‐actinCre Later | WT Hypoxia |
|---|---|---|---|---|
| Embryos examined | 26 | 21 | 16 | 15 |
| ASD* | — | — | 2 | |
| VSD* | — | 3 | 0 | 5 |
| PTA | 4 | — | 0 | — |
| DORV | 2 | — | 0 | 2 |
| Aorta over VSD | — | 4 | 0 | — |
The prevalence of cardiac defects in Wnt1Cre, β‐actinCre‐early and WT hypoxia groups were significantly different from controls (P<0.05). The prevalence of cardiac defects in β‐actinCre‐early vs. WT hypoxia were not significantly different (P=0.378). Data analyzed by Fisher's exact test. ASD indicates atrial septal defect; cKO, conditional knock‐out; DORV, double outlet right ventricle; Hif, hypoxia‐inducible transcription factor; PTA, persistent truncus arteriosus; VSD, ventricular septal defect; WT, wild type.
Embryos with isolated ASD and/or VSD. β‐actinCre early: Dams were given Tamoxifen (3 mg) at E10.5 and embryos examined at E15.5. β‐actinCre later: Dams were given Tamoxifen (3 mg) at E13.5 and embryos examined at E17.5.