Journal
PEDIATRIC SURGERY INTERNATIONAL
Volume 27, Issue 8, Pages 871-877Publisher
SPRINGER
DOI: 10.1007/s00383-011-2880-x
Keywords
Intestinal epithelial cells; Mitochondrial apoptotic signaling; Necrotizing enterocolitis; Oxidative stress; Reactive oxygen species; Growth factors
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Funding
- National Institutes of Health [R01 DK61470, R01 DK48498, P01 DK35608, T32 DK07639]
- Shriners Hospital for Children [8580]
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Reactive oxygen species (ROS) are thought to contribute to the pathogenesis of necrotizing enterocolitis (NEC). Mitochondria as a major source of intracellular ROS and apoptotic signaling during oxidative stress in NEC have not been investigated. We sought to determine: (1) the effects of oxidative stress on intestinal mitochondrial apoptotic signaling, and (2) the role of growth factors in this process. We used Swiss-Webster mice pups, and rat intestinal epithelial (RIE)-1, mitochondrial DNA-depleted RIE-1 cell line (RIE-1-rho A degrees) and human fetal intestinal epithelial cells (FHs74 Int) for our studies. H(2)O(2) induced apoptosis and ROS production. ROS-mediated activation of apoptotic signaling was significantly attenuated with mitochondrial silencing in RIE-1-rho A degrees cells. Growth factors, especially IGF-1, attenuated this response to H(2)O(2) in intestinal epithelial cells. Our findings suggest that mitochondria are a major source of intestinal apoptotic signaling during oxidative stress, and modulating mitochondrial apoptotic responses may help ameliorate the effects of NEC.
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