Lack of VEGFR2 signaling causes maldevelopment of the intestinal microvasculature and facilitates necrotizing enterocolitis in neonatal mice

Abstract

Plaen IG. Lack of VEGFR2 signaling causes maldevelopment of the intestinal microvasculature and facilitates necrotizing enterocolitis in neonatal mice.

Human Milk Fortification with Bovine Colostrum Is Superior to Formula‐Based Fortifiers to Prevent Gut Dysfunction, Necrotizing Enterocolitis, and Systemic Infection in Preterm Pigs

“…Inflammation and hypoxia may in synergy promote phagocytosis and release of antimicrobial peptides (ie, upregulation of PMAP23 ), and presumably affect intestinal integrity and microvascular network maybe via regulating VEGF signaling to compensate for the oxygen deficit . In this study, the effects on angiogenesis may have been limited as indicated by the slight (nonsignificant) upregulation of VEGFR2 , a primary receptor relaying VEGF signaling . Beyond the gut, FF feeding also leads to more systemic infections and potentially compromised immune capacity (ie, more bacteria resident in the bone marrow, reduced phagocytic capacity of blood neutrophils, and abnormal liver enzyme levels).…”

“…[30][31][32] In this study, the effects on angiogenesis may have been limited as indicated by the slight (nonsignificant) upregulation of VEGFR2, a primary receptor relaying VEGF signaling. 33 Beyond the gut, FF feeding also leads to more systemic infections and potentially compromised immune capacity (ie, more bacteria resident in the bone marrow, reduced phagocytic capacity of blood neutrophils, and abnormal liver enzyme levels 34 ). Total plasma postprandial AA levels were similar among groups, but the higher blood urea nitrogen values in the DHM+NAN group than in the DHM+BC group may reflect higher protein catabolism rates, which is probably related to increased systemic infections.…”

To transfuse or not transfuse a premature infant: the new complex question

“…These observations are biologically plausible, as early introduction of adult hemoglobin can cause an inadvertent shift in the oxygen dissociation curve, increasing oxygen delivery to tissues that are still developing adaptive mechanisms to tolerate increased oxygen concentrations [13]. The endothelial toxicity of oxygen in the developing retina is wellknown [14,15], and lends credence to these findings. While in existing studies, the link between ROP and RBC transfusions was noted in some [16,17], it was not evident in others [10,18,19]; these earlier studies did not focus on the timing of transfusion.…”

rhIGF-1/rhIGFBP-3 in preterm Infants: A phase 2 randomized controlled trial

“…Preclinical models indicate that IGF-I supplementation and subsequent enhancement of vascular endothelial growth factor receptor-2 signaling may have a preventive effect on development of NEC. [38][39][40][41][42] Higher levels of plasma IGF-1 were also associated with reduced incidence of NEC in a prospective analysis of very low birth weight infants in the NIRTURE study. 43 The administration of IGF-1/ IGFBP3 would not be expected to increase the risk of NEC.…”