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 Citations (Scopus)

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 2011

Fingerprint

Necrotizing Enterocolitis
Reactive Oxygen Species
Oxidative Stress
Epithelial Cells
Intercellular Signaling Peptides and Proteins
Mitochondria
Insulin-Like Growth Factor I
Mitochondrial DNA
Apoptosis
Cell Line

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

Cite this

Intestinal mitochondrial apoptotic signaling is activated during oxidative stress. / Baregamian, Naira; Song, Jun; Papaconstantinou, John; Hawkins, Hal K.; Evers, B. Mark; Chung, Dai H.

In: Pediatric Surgery International, Vol. 27, No. 8, 08.2011, p. 871-877.

Research output: Contribution to journalArticle

Baregamian, Naira ; Song, Jun ; Papaconstantinou, John ; Hawkins, Hal K. ; Evers, B. Mark ; Chung, Dai H. / Intestinal mitochondrial apoptotic signaling is activated during oxidative stress. In: Pediatric Surgery International. 2011 ; Vol. 27, No. 8. pp. 871-877.
@article{55bd1f8e7dd14809b311c2ca7d67101c,
title = "Intestinal mitochondrial apoptotic signaling is activated during oxidative stress",
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.",
keywords = "Growth factors, Intestinal epithelial cells, Mitochondrial apoptotic signaling, Necrotizing enterocolitis, Oxidative stress, Reactive oxygen species",
author = "Naira Baregamian and Jun Song and John Papaconstantinou and Hawkins, {Hal K.} and Evers, {B. Mark} and Chung, {Dai H.}",
year = "2011",
month = "8",
doi = "10.1007/s00383-011-2880-x",
language = "English (US)",
volume = "27",
pages = "871--877",
journal = "Pediatric Surgery International",
issn = "0179-0358",
publisher = "Springer Verlag",
number = "8",

}

TY - JOUR

T1 - Intestinal mitochondrial apoptotic signaling is activated during oxidative stress

AU - Baregamian, Naira

AU - Song, Jun

AU - Papaconstantinou, John

AU - Hawkins, Hal K.

AU - Evers, B. Mark

AU - Chung, Dai H.

PY - 2011/8

Y1 - 2011/8

N2 - 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.

AB - 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.

KW - Growth factors

KW - Intestinal epithelial cells

KW - Mitochondrial apoptotic signaling

KW - Necrotizing enterocolitis

KW - Oxidative stress

KW - Reactive oxygen species

UR - http://www.scopus.com/inward/record.url?scp=79961173427&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79961173427&partnerID=8YFLogxK

U2 - 10.1007/s00383-011-2880-x

DO - 10.1007/s00383-011-2880-x

M3 - Article

VL - 27

SP - 871

EP - 877

JO - Pediatric Surgery International

JF - Pediatric Surgery International

SN - 0179-0358

IS - 8

ER -