Primarily seen in premature infants, necrotizing enterocolitis (NEC) is the most common and most serious gastrointestinal disorder among hospitalized preterm infants. Despite improvements in clinical care and many previous clinical trials, the prognosis for newborns with NEC has not shown any significant improvement during the past 30 years and the mortality rate remains unchanged.
Investigators at Nationwide Children’s Hospital are focused on protecting the intestines from NEC, primarily by investigating molecular triggers and developing potential therapeutic targets such as growth factors that may serve as cytoprotective agents against intestinal damage.
HB-EGF Protects Intestinal Stem Cells from Injury
Various forms of intestinal injury, including necrotizing enterocolitis injure the intestinal epithelial cell lineages, including the intestinal stem cells (ISCs). This disrupts the normal balance needed to maintain gut barrier function. This study suggests that the growth factor HB-EGF protects the intestine at least in part through its ability to protect ISCs from injury.
Access an abstract of this study: Heparin-binding EGF-like growth factor protects intestinal stem cells from injury in a rat model of necrotizing enterocolitis. Lab Invest. 2011 Dec 12. doi: 10.1038/labinvest.2011.167. [Epub ahead of print]
How HB-EGF Reduces Inflammation and Preserves Gut Barrier Function after Injury
This study explores the mechanisms underlying the anti-inflammatory role that the growth factor HB-EGF has on preserving gut barrier function after injury.
Access an abstract of this study: Heparin-binding epidermal growth factor-like growth factor (HB-EGF) preserves gut barrier function by blocking neutrophil-endothelial cell adhesion after hemorrhagic shock and resuscitation in mice. Surgery. 2011 Dec 7. [Epub ahead of print]
Poly(ADP-ribose) Polymerase-1: A Novel Therapeutic Target in Necrotizing Enterocolitis
Inflammation and oxidation may be involved in NEC. The enzyme Poly(ADP-ribose) polymerase-1 (PARP-1) assists in DNA repair. However, when oxidative stress and DNA damage happen, PARP-1 may over-activate and deplete cells of NAD+ and ATP, which kills the cells. We speculate that PARP-1 overactivation in NEC may drive cell death in this disease and that PARP-1 may be a novel therapeutic target in NEC.
Access an abstract of this study: Poly(ADP-ribose) polymerase-1: a novel therapeutic target in necrotizing. Pediatr Res. 2011 Jul;70(1):67-71.
Establishing a Biologic Signature for Necrotizing Enterocolitis, Sepsis, and Inflammation in the Neonate, Anonymous (Lawrence Moss)
The Comparative Effectiveness of Laparotomy versus Drain Placement in Extremely Low Birth Weight Infants with Necrotizing Enterocolitis, The Ohio State University (Jonathan Slaughter)
HB-EGF and Intestinal Ischemia/Reperfusion, National Institutes of Health (Gail Besner)
Novel Complementary Therapy for Preterm Infants, Anonymous (Peter Giannone)
Fetal Origins of Necrotizing Enterocolitis, March of Dimes (Peter Giannone)
Newly-Recruited Surgeon-in-Chief Has Research Interests in NEC
R. Lawerence Moss, MD, brings national leadership of a multi-institutional research network studying necrotizing enterocolitis.
Read more :: Moss Appointed Surgeon in Chief at Nationwide Children’s
Dr. Besner Receives Endowed Chair in Neonatal Research
For clinicians and researchers working in academic-medical institutions, endowed chairs represent the most prestigious and significant recognition of their work.
Read more: Dr. Besner Receives Endowed Chair