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Intestinal mitochondrial apoptotic signaling is activated during oxidative stress.
- Source :
-
Pediatric Surgery International . Aug2011, Vol. 27 Issue 8, p871-877. 7p. 4 Graphs. - Publication Year :
- 2011
-
Abstract
- <bold>Purpose: </bold>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.<bold>Methods: </bold>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.<bold>Results: </bold>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.<bold>Conclusions: </bold>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. [ABSTRACT FROM AUTHOR]
- Subjects :
- *MITOCHONDRIA
*APOPTOSIS
*CELLULAR signal transduction
*OXIDATIVE stress
*REACTIVE oxygen species
*NEONATAL necrotizing enterocolitis
*GROWTH factors
*EPITHELIAL cells
*ANIMAL experimentation
*ANIMAL populations
*CELL culture
*COMPARATIVE studies
*DNA
*ENZYME-linked immunosorbent assay
*FLOW cytometry
*INTESTINAL mucosa
*SMALL intestine
*RESEARCH methodology
*MEDICAL cooperation
*MICE
*RATS
*RESEARCH
*WESTERN immunoblotting
*EVALUATION research
Subjects
Details
- Language :
- English
- ISSN :
- 01790358
- Volume :
- 27
- Issue :
- 8
- Database :
- Academic Search Index
- Journal :
- Pediatric Surgery International
- Publication Type :
- Academic Journal
- Accession number :
- 62661901
- Full Text :
- https://doi.org/10.1007/s00383-011-2880-x