Intestinal mitochondrial apoptotic signaling is activated during oxidative stress.
Intestinal mitochondrial apoptotic signaling is activated during oxidative stress.
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DOI：
10.1007/s00383-011-2880-x
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发表时间：
2011-08
影响因子：
1.8
通讯作者：
Chung DH
中科院分区：
文献类型：
--
作者：
Baregamian N;Song J;Papaconstantinou J;Hawkins HK;Evers BM;Chung DH
活性氧（ROS）被认为是坏死性小肠结肠炎（NEC）的发病机制。线粒体作为NEC中氧化应激过程中细胞内ROS和凋亡信号的主要来源尚未研究。我们试图确定：（1）氧化应激对肠线粒体凋亡信号的影响，以及（2）生长因子在此过程中的作用。我们使用Swiss韦伯斯特小鼠幼仔、大鼠肠上皮细胞（RIE-1）、线粒体DNA缺失的RIE-1细胞系（RIE-1-ρ°）和人胎儿肠上皮细胞（FHS 74 Int）进行研究。H2 O2诱导细胞凋亡和ROS产生。ROS介导的凋亡信号的激活在RIE-1-ρ°细胞中被线粒体沉默显著减弱。生长因子，特别是IGF-1，减弱这种反应，过氧化氢在肠上皮细胞。我们的研究结果表明，线粒体是氧化应激过程中肠细胞凋亡信号的主要来源，调节线粒体凋亡反应可能有助于改善NEC的影响。
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-ρ°) and human fetal intestinal epithelial cells (FHs74 Int) for our studies. H2O2 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 H2O2 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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影响因子：
29.4
作者：
KESHAVARZIAN, A;SEDGHI, S;WINSHIP, D
通讯作者：
WINSHIP, D
影响因子：
2.2
作者：
Baregamian, Naira;Song, Jun;Chung, Dai H.
通讯作者：
Chung, Dai H.
影响因子：
2.9
作者：
BRADFORD, MM
通讯作者：
BRADFORD, MM
影响因子：
24.5
作者：
KESHAVARZIAN, A;MORGAN, G;DORIA, M
通讯作者：
DORIA, M
影响因子：
1.9
作者：
D'Odorico, A;Bortolan, S;Sturniolo, GC
通讯作者：
Sturniolo, GC