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

The pathogenesis of necrotizing enterocolitis (NEC), a common gastrointestinal disease affecting premature infants, remains poorly understood. We previously found that intestinal VEGF-A expression is decreased in human NEC samples and in a neonatal mouse NEC model prior to detectable histological injury. Therefore, we hypothesized that lack of VEGF receptor 2 (VEGFR2) signaling facilitates neonatal intestinal injury by impairing intestinal microvasculature development.

Characterization of a necrotizing enterocolitis model in newborn mice.

Background: Necrotizingenterocolitis (NEC) is a major health concern for premature infants and its patho-genesis remains poorly understood. The current mouse NEC model has not well been characterized.

Objectives: In this study, we develop a simple mouse model of NEC and determine the role of several factors modulating human NEC (i.