Document Detail


Intestinal mitochondrial apoptotic signaling is activated during oxidative stress.
MedLine Citation:
PMID:  21400030     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
PURPOSE: 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. METHODS: We used Swiss-Webster mice pups, and rat intestinal epithelial (RIE)-1, mitochondrial DNA-depleted RIE-1 cell line (RIE-1-ρ°) and human fetal intestinal epithelial cells (FHs74 Int) for our studies. RESULTS: H(2)O(2) induced apoptosis and ROS production. ROS-mediated activation of apoptotic signaling was significantly attenuated with mitochondrial silencing in RIE-1-ρ° cells. Growth factors, especially IGF-1, attenuated this response to H(2)O(2) in intestinal epithelial cells. CONCLUSIONS: 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.
Authors:
Naira Baregamian; Jun Song; John Papaconstantinou; Hal K Hawkins; B Mark Evers; Dai H Chung
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-3-13
Journal Detail:
Title:  Pediatric surgery international     Volume:  -     ISSN:  1437-9813     ISO Abbreviation:  -     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-3-14     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8609169     Medline TA:  Pediatr Surg Int     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Department of Surgery, The University of Texas Medical Branch, Galveston, TX, 77555, USA.
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