Vascular Endothelial Growth Factor Protein is Decreased in a Mouse Model of Necrotizing Enterocolitis

Abstract

Necrotizing enterocolitis (NEC) is a severe intestinal disease affecting premature infants. Its pathogenesis remains poorly understood. Vascular endothelial growth factor (VEGF) is an angiogenic protein that plays a role in several pathologic processes. While VEGF polymorphisms have been associated with NEC, the role of VEGF in the pathogenesis of NEC remains unknown. Here, we examined the developmental expression of VEGF in the mouse intestine and in a neonatal mouse NEC model. To determine VEGF developmental expression, pups were sacrificed at embryonic day (E) 16, postnatal day (D) 0 or 3. To examine intestinal VEGF in our NEC model, animals were submitted to the NEC protocol for 48 hours or allowed to be dam fed. Intestinal VEGF protein was assessed by western blot followed by band densitometry (values were normalized to β‐actin). Compared to D0, only a low amount of VEGF was detected in the mouse intestine at E16 (2.6±0.42 % of D0 value; p<0.05). At D3, there was a marginal increase in VEGF compared to D0 (194 ±20 %), although this was not statistically significant. In pups exposed to the NEC protocol, intestinal VEGF was not detectable while it was strongly present in dam fed controls. In conclusion, we found that intestinal VEGF is increased after birth in dam fed pups, but undetectable at 48 hours in our neonatal mouse NEC model. Therefore, we speculate that VEGF plays a role in the pathogenesis of this disease.