Prostanoids, not reactive oxygen species, mediate COX-2-dependent neurotoxicity

2004 ◽  
Vol 55 (5) ◽  
pp. 668-675 ◽  
Author(s):  
Yasuhiro Manabe ◽  
Josef Anrather ◽  
Takayuki Kawano ◽  
Kiyoshi Niwa ◽  
Ping Zhou ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cox 2

scholarly journals Up-regulation of glomerular COX-2 by angiotensin II: Role of reactive oxygen species

2005 ◽  
Vol 68 (5) ◽  
pp. 2143-2153 ◽  
Author(s):  
Edgar A. Jaimes ◽  
Run-Xia Tian ◽  
Damien Pearse ◽  
Leopoldo Raij
Keyword(s):  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cox 2

scholarly journals Hypertonic Induction of COX-2 in Collecting Duct Cells by Reactive Oxygen Species of Mitochondrial Origin

2005 ◽  
Vol 280 (41) ◽  
pp. 34966-34973 ◽  
Author(s):  
Tianxin Yang ◽  
Aihua Zhang ◽  
Matthew Honeggar ◽  
Donald E. Kohan ◽  
Diane Mizel ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Collecting Duct ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Duct Cells ◽  
Collecting Duct Cells ◽  
Mitochondrial Origin ◽  
Cox 2

scholarly journals Reactive oxygen species induce Cox-2 expression via TAK1 activation in synovial fibroblast cells

FEBS Open Bio ◽  
2015 ◽  
Vol 5 (1) ◽  
pp. 492-501 ◽  
Author(s):  
Yuta Onodera ◽  
Takeshi Teramura ◽  
Toshiyuki Takehara ◽  
Kanae Shigi ◽  
Kanji Fukuda
Keyword(s):  
Reactive Oxygen Species ◽  
Synovial Fibroblast ◽  
Reactive Oxygen ◽  
Fibroblast Cells ◽  
Oxygen Species ◽  
Cox 2

scholarly journals Transcriptional Regulation of Cyclooxygenase-2 in Response to Proteasome Inhibitors Involves Reactive Oxygen Species-mediated Signaling Pathway and Recruitment of CCAAT/Enhancer-binding Protein δ and CREB-binding Protein

2005 ◽  
Vol 16 (12) ◽  
pp. 5579-5591 ◽  
Author(s):  
Jun-Jie Chen ◽  
Wei-Chien Huang ◽  
Ching-Chow Chen
Keyword(s):  
Reactive Oxygen Species ◽  
Gene Transcription ◽  
Binding Protein ◽  
Proteasome Inhibitors ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Creb Binding Protein ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein ◽  
Cox 2

Inhibition of ubiquitin-proteasome pathway has been shown to be a promising strategy for the treatment of inflammation and cancer. Here, we show that proteasome inhibitors MG132, PSI-1, and lactacystin induce COX-2 expression via enhancing gene transcription rather than preventing protein degradation in the human alveolar NCI-H292 and A549, and gastric AGS epithelial cells. NF-IL6 and CRE, but not NF-κB elements on the COX-2 promoter were involved in the gene transcription event. The binding of CCAAT/enhancer binding protein (C/EBP)β and C/EBPδ to the CRE and NF-IL6 elements, as well as the recruitment of CBP and the enhancement of histone H3 and H4 acetylation on the COX-2 promoter was enhanced by MG132. However, it did not affect the total protein levels of C/EBPβ and C/EBPδ. MG132-induced DNA-binding activity of C/EBPδ, but not C/EBPβ was regulated by p38, PI3K, Src, and protein kinase C. Small interfering RNA of C/EBPδ suppressed COX-2 expression, further strengthening the role of C/EBPδ in COX-2 gene transcription. In addition, the generation of intracellular reactive oxygen species (ROS) in response to MG132 contributed to the activation of MAPKs and Akt. These findings reveal that the induction of COX-2 transcription induced by proteasome inhibitors requires ROS-dependent protein kinases activation and the subsequent recruitments of C/EBPδ and CBP.

Contribution of reactive oxygen species to migration/invasion of human glioblastoma cells U87 via ERK-dependent COX-2/PGE2 activation

2010 ◽  
Vol 37 (1) ◽  
pp. 118-129 ◽  
Author(s):  
Wen-Ta Chiu ◽  
Shing-Chuan Shen ◽  
Jyh-Ming Chow ◽  
Cheng-Wei Lin ◽  
Ling-Tin Shia ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Glioblastoma Cells ◽  
Human Glioblastoma ◽  
Cox 2 ◽  
Human Glioblastoma Cells

scholarly journals Reactive Oxygen Species Mediated Prostaglandin E2 Contributes to Acute Response of Epithelial Injury

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Yi-Ping Hu ◽  
Yin-Bo Peng ◽  
Yi-Fan Zhang ◽  
Ying Wang ◽  
Wei-Rong Yu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Tissue Injury ◽  
Reactive Oxygen ◽  
Human Keratinocytes ◽  
Mechanical Injury ◽  
Prostaglandin E ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Cox 2

Reactive oxygen species (ROS) generated after tissue injury play a crucial role during wound healing through initiating acute inflammation, clarifying infection and dead tissue, and mediating various intracellular signal transduction. Prostaglandin E2 (PGE2) has been identified as one of the major factors responsible for inflammation and tissue repair. In this study, we tested our hypothesis that ROS produced by damaged human keratinocytes induces the synthesis of PGE2. In vitro epithelial wounding model was used to observe the production of ROS and secretion of PGE2 as well as the involved signal pathway. The mechanical injury caused the rapid production of ROS in in vitro cultured keratinocytes, which was significantly blocked by an inhibitor of nicotinamide adenine dinucleotide phosphate oxidase. The increased intracellular ROS caused by mechanical injury stimulates PGE2 production in a time-dependent manner via the activation of cyclooxygenase-2 (COX-2), which was stimulated by phosphorylation of extracellular signal-regulated protein kinase (ERK). These results indicate ROS-induced ERK activation leading to the activation of COX-2 and the synthesis of PGE2 in human keratinocytes responding to mechanical injury in the acute phase.

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