Intestinal mitochondrial apoptotic signaling is activated during oxidative stress

Naira Baregamian, Jun Song, John Papaconstantinou, Hal K. Hawkins, B. Mark Evers, Dai H. Chung

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

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 2O 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 2O 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.

Original languageEnglish (US)
Pages (from-to)871-877
Number of pages7
JournalPediatric Surgery International
Volume27
Issue number8
DOIs
StatePublished - Aug 1 2011

Keywords

  • Growth factors
  • Intestinal epithelial cells
  • Mitochondrial apoptotic signaling
  • Necrotizing enterocolitis
  • Oxidative stress
  • Reactive oxygen species

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Surgery

Fingerprint Dive into the research topics of 'Intestinal mitochondrial apoptotic signaling is activated during oxidative stress'. Together they form a unique fingerprint.

  • Cite this