Tumor Necrosis Factor-α and Apoptosis Signal-Regulating Kinase 1 Control Reactive Oxygen Species Release, Mitochondrial Autophagy and C-Jun N-Terminal Kinase/P38 Phosphorylation During Necrotizing Enterocolitis | Zendy

Naira Baregamian | Zendy; Jun Song | Zendy; Christopher E. Bailey | Zendy; John Papaconstantinou | Zendy; Bret M. Evers | Zendy; Dai H. Chung | Zendy

Open Access

Tumor Necrosis Factor-α and Apoptosis Signal-Regulating Kinase 1 Control Reactive Oxygen Species Release, Mitochondrial Autophagy and C-Jun N-Terminal Kinase/P38 Phosphorylation During Necrotizing Enterocolitis

Author(s) -

Naira Baregamian,

Jun Song,

Christopher E. Bailey,

John Papaconstantinou,

Bret M. Evers,

Dai H. Chung

Publication year - 2009

Publication title -

oxidative medicine and cellular longevity

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.494

H-Index - 93

eISSN - 1942-0900

pISSN - 1942-0994

DOI - 10.4161/oxim.2.5.9541

Subject(s) - reactive oxygen species , microbiology and biotechnology , mitochondrial ros , tumor necrosis factor alpha , p38 mitogen activated protein kinases , apoptosis , biology , mitochondrion , ask1 , oxidative stress , autophagy , kinase , programmed cell death , cancer research , protein kinase a , cyclin dependent kinase 2 , immunology , biochemistry

Oxidative stress and inflammation may contribute to the disruption of the protective gut barrier through various mechanisms; mitochondrial dysfunction resulting from inflammatory and oxidative injury may potentially be a significant source of apoptosis during necrotizing enterocolitis (NEC). Tumor necrosis factor (TNF)-alpha is thought to generate reactive oxygen species (ROS) and activate the apoptosis signal-regulating kinase 1 (ASK1)-c-Jun N-terminal kinase (JNK)/p38 pathway. Hence, the focus of our study was to examine the effects of TNF-alpha/ROS on mitochondrial function, ASK1-JNK/p38 cascade activation in intestinal epithelial cells during NEC.

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