Ethanol-induced oxidative stress is mediated by p38 MAPK pathway in mouse hippocampal cells

Ku, Bo Mi; Lee, Yeon Kyung; Jeong, Joo; Mun, Jihye; Han, Jae Yoon; Roh, Gu Seob; Kim, Hyun Joon; Cho, Gyeong Jae; Choi, Wan Sung; Yi, Gwan‐Su; Kang, Sang Soo

doi:10.1016/j.neulet.2007.03.049

Cited by 60 publications

(39 citation statements)

References 20 publications

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“…In addition, the effect of ethanol on pro-survival pathways may depend on the differentiation state of the cells examined. Developing neurons are more sensitive to inhibition of Akt by ethanol (Chandler and Sutton, 2005), certain transformed cells show an increase in ERK activation in response to chronic ethanol exposure (Roivainen et al, 1995;Ku et al, 2007), while terminally differentiated cells, for the most part, show inhibition of ERK after acute exposure Chandler and Sutton, 2005;Li et al, 2004;Ohrtman et al, 2006). Detailed temporal, global immunohistochemical mapping studies of activated protein kinases, neuronal activity and the determination of neuronal identities will be essential in resolving temporal and regional differences.…”

Section: Effects Of Etoh On Bdnf Signalingmentioning

confidence: 99%

Ethanol–BDNF interactions: Still more questions than answers

Davis

2008

Pharmacology & Therapeutics

126

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Brain Derived Neurotrophic Factor (BDNF) has emerged as a regulator of development, plasticity and, recently, addiction. Decreased neurotrophic activity may be involved in ethanol-induced neurodegeneration in the adult brain and in the etiology of alcohol-related neurodevelopmental disorders. This can occur through decreased expression of BDNF or through inability of the receptor to transduce signals in the presence of ethanol. In contrast, recent studies implicate region-specific up-regulation of BDNF and associated signaling pathways in anxiety, addiction and homeostasis after ethanol exposure. Anxiety and depression are precipitating factors for substance abuse and these disorders also involve region-specific changes in BDNF in both pathogenesis and response to pharmacotherapy. Polymorphisms in the genes coding for BDNF and its receptor TrkB are linked to affective, substance abuse and appetitive disorders and therefore may play a role in the development of alcoholism. This review summarizes historical and pre-clinical data on BDNF and TrkB as it relates to ethanol toxicity and addiction. Many unresolved questions about region-specific changes in BDNF expression and the precise role of BDNF in neuropsychiatric disorders and addiction remain to be elucidated. Resolution of these questions will require significant integration of the literature on addiction and comorbid psychiatric disorders that contribute to the development of alcoholism.

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Section: Effects Of Etoh On Bdnf Signalingmentioning

confidence: 99%

Ethanol–BDNF interactions: Still more questions than answers

Davis

2008

Pharmacology & Therapeutics

126

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“…Many studies have reported the role of stress-activated protein kinases such as p38/MAPK [18,23,25,52] and ERK [1,34,54] in the generation and modulation of oxidative stress responses. In order to investigate whether visfatin-induced oxidative stress in myocytes was associated with activation of MAPK signalling, we investigated phosphorylation of p38 and ERK proteins by Western blot analysis.…”

Section: Visfatin-induced Generation Of Oxidative Stress Occurs Indepmentioning

confidence: 99%

Visfatin induces oxidative stress in differentiated C2C12 myotubes in an Akt- and MAPK-independent, NFĸB-dependent manner

Oita

Ferdinando

Wilson

et al. 2009

Pflugers Arch - Eur J Physiol

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Adipose tissue is an important endocrine and metabolic tissue that is actively involved in cross-talk with peripheral organs such as skeletal muscle. It is likely that adipose-derived factors may underlie the development of insulin resistance in muscle. Thus, the cross-talk between adipose and muscle may be important for the propagation of obesity-related diseases. Visfatin (Pre-B-cell colony-enhancing factor 1 homolog/Nampt) is a recently discovered adipokine with pleiotropic functions. The aim of this study was to examine the effect of visfatin on cellular stress responses and signalling pathways in skeletal muscle. Visfatin treatment of differentiated C2C12 myotubes generated reactive oxygen species (ROS) comprising both superoxide and hydrogen peroxide that was dependent on de novo transcription and translation. In differentiated C2C12 myoblasts, visfatin had no effects on insulin-stimulated Akt phosphorylation nor on activation of the Akt signalling pathway. Additionally, visfatin-induced oxidative stress occurred independent of activation of the stress-activated protein kinases (MAPKs) ERK and p38. In contrast, phosphorylation of NFkB was associated with visfatin-mediated generation of ROS and blockade of this pathway via selective IKK inhibition led to a partial reduction in oxidative stress. Furthermore, the generation of ROS following visfatin treatment was highly dependent on both de novo transcription and translation. Taken together, these findings provide novel insights for the unique pathophysiological role of visfatin in skeletal muscle.

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“…The ERK1/2 pathways, which are thought to be triggered preferentially by growth factors and mitogens, play an important role during development in the regulation of cell proliferation and differentiation (Turjanski et al, 2007). Activation of the p38 and JNK MAPKs is triggered by stimuli ranging from growth factors to a variety of stress stimuli, including intracellular pH changes, ultraviolet irradiation, heat shock, DNA-damaging agents, hyperglycemia, ethanol, hypoxia, and oxidative stress (Kyriakis and Avruch, 1996;Ku et al, 2007). Stress-response MAPKs control defense responses that determine whether cells survive, differentiate, or apoptose.…”

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confidence: 99%

“…During limb development, bone morphogenetic proteins activate p38 MAPK in interdigital tissues undergoing regression, up-regulating some of the genes that mediate programmed cell death (Zuzarte-Luís et al, 2004). However, p38 MAPK has an opposite role in neuronal cells in vitro: inhibitors of p38 promote cell survival (Horstmann et al, 1998) and have been reported to protect hippocampal cells against ethanol cytotoxicity (Ku et al, 2007). The mechanism by which inhibition of p38 MAPK activation is detrimental in one system, or at one time during development, and plays a protective role elsewhere remains to be determined.…”

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confidence: 99%