ArticleJournal of pediatric surgery2010
Heparin-binding epidermal growth factor-like growth factor overexpression in transgenic mice increases resistance to necrotizing enterocolitis.
Article in Journal of pediatric surgery, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 38 citations in OpenAlex.
- Exosomes derived from colostrum and mature human breast milk protect against experimental necrotizing enterocolitis.Pediatric surgery international · 2025Article
- Effect of prenatal heparin-binding epidermal growth factor (HB-EGF) administration on necrotizing enterocolitis-induced lung injury in a murine model.World journal of pediatric surgery · 2025Article
- Prenatal administration of heparin-binding epidermal growth factor-like growth factor in an experimental model of necrotizing enterocolitis decreased both incidence and severity of the disease.World journal of pediatric surgery · 2022Article
- Prenatal stress increases IgA coating of offspring microbiota and exacerbates necrotizing enterocolitis-like injury in a sex-dependent manner.Brain, behavior, and immunity · 2020Article
- Saccharomyces boulardii modulates necrotizing enterocolitis in neonatal mice by regulating the sirtuin 1/NF‑κB pathway and the intestinal microbiota.Molecular medicine reports · 2020Article
- Animal models of necrotizing enterocolitis.World journal of pediatric surgery · 2020Review
- Maternal IgA protects against the development of necrotizing enterocolitis in preterm infants.Nature medicine · 2019Article
- Genetic predisposition to necrotizing enterocolitis in premature infants: Current knowledge, challenges, and future directions.Seminars in fetal & neonatal medicine · 2018Review
- Heparin-binding EGF-like growth factor promotes neuronal nitric oxide synthase expression and protects the enteric nervous system after necrotizing enterocolitis.Pediatric research · 2017Article
- The Role of Mucosal Immunity in the Pathogenesis of Necrotizing Enterocolitis.Frontiers in pediatrics · 2017Review
- Formula feeding and systemic hypoxia synergistically induce intestinal hypoxia in experimental necrotizing enterocolitis.Pediatric surgery international · 2016Article
- The viral dsRNA analogue poly (I:C) induces necrotizing enterocolitis in neonatal mice.Pediatric research · 2016Article
- A spectrum of intestinal injury models in neonatal mice.Pediatric surgery international · 2016Article
- Necrotizing enterocolitis in a mouse model leads to widespread renal inflammation, acute kidney injury, and disruption of renal tight junction proteins.Pediatric research · 2015Article
- M1 to M2 macrophage polarization in heparin-binding epidermal growth factor-like growth factor therapy for necrotizing enterocolitis.The Journal of surgical research · 2015Article
- Early maternal separation induces alterations of colonic epithelial permeability and morphology.Pediatric surgery international · 2014Article
- The ErbB4 ligand neuregulin-4 protects against experimental necrotizing enterocolitis.The American journal of pathology · 2014Article
- Argininosuccinate lyase in enterocytes protects from development of necrotizing enterocolitis.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Heparin-binding EGF-like growth factor (HB-EGF) promotes cell migration and adhesion via focal adhesion kinase.The Journal of surgical research · 2014Article
- Heparin-binding EGF-like growth factor (HB-EGF) therapy for intestinal injury: Application and future prospects.Pathophysiology : the official journal of the International Society for Pathophysiology · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundNecrotizing enterocolitis (NEC) is the most common gastrointestinal emergency and the leading surgical cause of death in premature infants. We have shown that administration of exogenous heparin-binding epidermal growth factor-like growth factor (HB-EGF) in mice protects the intestines from experimental NEC. The aim of the current study was to evaluate the effect of gain-of-function of endogenous HB-EGF on susceptibility to NEC.
methodsNeonatal HB-EGF transgenic (TG) mice and their wild-type (WT) counterparts were exposed to experimental NEC. An additional group of HB-EGF TG pups were also exposed to NEC, but received the HB-EGF antagonist cross-reacting material 197 (CRM197) injected subcutaneously immediately after birth. To examine gut barrier function, HB-EGF TG and WT pups received intragastric fluorescein isothiocyanate-labeled dextran under basal and stressed conditions, and serum fluorescein isothiocyanate-labeled dextran levels were measured.
resultsWild-type mice had an incidence of NEC of 54.2%, whereas HB-EGF TG mice had a significantly decreased incidence of NEC of 22.7% (P = .03). Importantly, administration of CRM197 to HB-EGF TG pups significantly increased the incidence of NEC to 65% (P = .004). HB-EGF TG mice had significantly decreased intestinal permeability compared to WT mice both under basal and stressed conditions.
conclusionsOur results provide evidence that overexpression of the HB-EGF gene decreases susceptibility to NEC and that administration of the HB-EGF antagonist CRM197 reverses this protective effect.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.