| First Author | Cai LX | Year | 2020 |
| Journal | Dev Dyn | Volume | 249 |
| Issue | 5 | Pages | 636-645 |
| PubMed ID | 31900966 | Mgi Jnum | J:287407 |
| Mgi Id | MGI:6415416 | Doi | 10.1002/dvdy.149 |
| Citation | Cai LX, et al. (2020) Defective coronary vessel organization and reduction of VEGF-A in mouse embryonic hearts with gestational mild hypoxia. Dev Dyn 249(5):636-645 |
| abstractText | BACKGROUND: Vasculature is formed by responding to homeostatic tissue demands including in developing hearts. Hypoxia generally stimulates vascular formation in which vascular endothelial growth factor A (VEGF-A) plays a critical role. Gestational hypoxia increases the risk of low intrauterine growth and low birth weight, both of which are known to increase the risk of the fetus developing cardiovascular defects. In fact, continuous gestational mild hypoxia (14% O2 ) from the mid-embryonic stage causes cardiac anomalies accompanied by a thinning compact layer in mice in vivo. Because coronary vasculature formation is necessary for compact layers to thicken, we hypothesized that defective coronary vessel organization is related to the thinning compact layer under gestational hypoxia conditions. RESULTS: Continuous gestational mild hypoxia (14% O2 ) applied from embryonic day 10.5 (E10.5) reduced the expression of VEGF-A mRNA and proteins by over 60% in E12.5 hearts relative to control normoxic hearts. Formation of CD31-positive vascular plexus, blood islands, and microvessels in embryonic ventricles were stunted by gestational hypoxia compared to control E12.5 hearts. CONCLUSIONS: Our results suggest that mild hypoxia (14% O2 ) does not induce coronary vessel organization or VEGF-A expression in developing mouse hearts, opposing the general effects of hypoxia-triggering vascular organization and VEGF-A expression. |
