Redox-sensitive protein phosphatase activity regulates the phosphorylation state of p38 protein kinase in primary astrocyte culture

Robinson, Kent A.; Stewart, Charles A.; Pye, Quentin N.; Nguyen, Xuan Canh; Kenney, Lauren; Salzman, Scott; Floyd, Robert A.; Hensley, Kenneth

doi:10.1002/(sici)1097-4547(19990315)55:6<724::aid-jnr7>3.0.co;2-9

Cited by 99 publications

(46 citation statements)

References 40 publications

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“…After PC12 cells were pretreated with SB203580 prior to exposure to CoCl 2 , CoCl 2 -induced ROS production was markedly blocked, suggesting that p38MAPK may be a positive regulator for CoCl 2 -induced ROS production in PC12 cells. Previous studies reported that ROS appeared to be upstream of p38MAPK (33). However, based on our results, ROS and p38MAPK may locate at a parallel level, and there is interaction between ROS and p38MAPK during CoCl 2 -induced neuronal injuries.…”

supporting

confidence: 44%

Interaction between ROS and p38MAPK contributes to chemical hypoxia-induced injuries in PC12 cells

et al. 2011

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Abstract. The present study investigated whether there is an interaction between reactive oxygen species (ROS) and p38 mitogen-activated protein kinase (MAPK) during chemical hypoxia-induced injury in PC12 cells. The results of the present study showed that cobalt chloride (CoCl 2 ), a chemical hypoxia agent, markedly induced ROS generation and phosphorylation of p38MAPK, as well as neuronal injuries. N-acetylcysteine (NAC), a ROS scavenger, blocked CoCl 2 -induced phosphorylation of p38MAPK. In addition, SB203580, an inhibitor of p38MAPK attenuated not only CoCl 2 -induced activation of p38MAPK, but also ROS production. These results suggest that ROS and p38MAPK are capable of interacting positively during chemical hypoxia. Furthermore, NAC and SB203580 markedly prevented CoCl 2 -induced cytotoxicity, apoptosis and a loss of mitochondrial membrane potential. Taken together, our findings suggest that the positive interaction between CoCl 2 induction of ROS and p38MAPK activation may play a significant role in CoCl 2 -induced neuronal injuries. We provide new insights into the mechanisms responsible for CoCl 2 -induced injuries in PC12 cells.

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supporting

confidence: 44%

Interaction between ROS and p38MAPK contributes to chemical hypoxia-induced injuries in PC12 cells

et al. 2011

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“…In particular, p38 and JNK have critical roles in the inflammatory response and are regulated by various pro-inflammatory cytokines [42,43] and ROS [56,60]. To assess the effects of ROS on intracellular signaling, we evaluated P2X 7 agonist-initiated events following treatment of cells with the anti-oxidants ascorbic acid and NAC, which function by increasing intracellular glutathione and reducing oxidized proteins [57].…”

Section: Discussionmentioning

confidence: 99%

Nucleotide receptor signaling in murine macrophages is linked to reactive oxygen species generation

Pfeiffer

Guerra

Hill

et al. 2007

Free Radical Biology and Medicine

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Macrophage activation is critical in the innate immune response and can be regulated by the nucleotide receptor P2X 7 . In this regard, P2X 7 signaling is not well understood but has been implicated in controlling reactive oxygen species (ROS) generation by various leukocytes. Although ROS can contribute to microbial killing, the role of ROS in nucleotide-mediated cell signaling is unclear. In this study, we report that the P2X 7 agonists ATP and 3′-O-(4-benzoyl) benzoic ATP (BzATP) stimulate ROS production by RAW 264.7 murine macrophages. These effects are potentiated in lipopolysaccharide-primed cells, demonstrating an important interaction between extracellular nucleotides and microbial products in ROS generation. In terms of nucleotide receptor specificity, RAW 264.7 macrophages that are deficient in P2X 7 are greatly reduced in their capacity to generate ROS in response to BzATP treatment (both with and without LPS priming), thus supporting a role for P2X 7 in this process. Because MAP kinase activation is key for nucleotide regulation of macrophage function, we also tested the hypothesis that P2X 7 -mediated MAP kinase activation is dependent on ROS production. We observed that BzATP stimulates MAP kinase (ERK1/ ERK2, p38, and JNK1/JNK2) phosphorylation, and that the antioxidants N-acetyl-cysteine and ascorbic acid strongly attenuate BzATP-mediated JNK1/JNK2 and p38 phosphorylation but only slightly reduce BzATP-induced ERK1/ERK2 phosphorylation. These studies reveal that P2X 7 can contribute to macrophage ROS production, that this effect is potentiated upon lipopolysaccharide exposure, and that ROS are important participants in the extracellular nucleotide-mediated activation of several MAP kinase systems.

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“…IL-1␤ has been found to elicit H 2 O 2 synthesis in rat primary astrocytes [16] and IL-1␤ mRNA is increased by NADPH oxidase-derived ROS in rat primary astrocyte and microglia cultures [14]. Cortical COX-2 has also been reported to be markedly increased, and high levels of ROS generated in response to a high fat diet, suggesting a neural inflammatory response [32].…”

mentioning

confidence: 99%

Immobilization stress induces cell death through production of reactive oxygen species in the mouse cerebral cortex

Choi

Lee

Choi

et al. 2006

Neuroscience Letters

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Redox-sensitive protein phosphatase activity regulates the phosphorylation state of p38 protein kinase in primary astrocyte culture

Cited by 99 publications

References 40 publications

Interaction between ROS and p38MAPK contributes to chemical hypoxia-induced injuries in PC12 cells

Interaction between ROS and p38MAPK contributes to chemical hypoxia-induced injuries in PC12 cells

Nucleotide receptor signaling in murine macrophages is linked to reactive oxygen species generation

Immobilization stress induces cell death through production of reactive oxygen species in the mouse cerebral cortex

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