Involvement of Lipid Peroxidation in the Alteration of Protein Kinase C Signaling

Takekoshi, Susumu; Nagata, Hidetaka; Matsuzaki, Kei; Osamura, R. Yoshiyuki

doi:10.1267/ahc.36.281

Cited by 7 publications

(4 citation statements)

References 47 publications

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“…Analysis by qPCR confirmed that Gsta4 was expressed at levels more than 20‐fold greater in epidermis of C57BL/6J versus DBA/2J mice following TPA treatment. This glutathione transferase appears to play a significant role in detoxification of 4‐hydroxy‐2‐nonenal (4‐HNE), a byproduct of lipid peroxidation which accumulates in the epidermis after TPA treatment [76–78]. In this regard, Gsta4 reportedly catalyzes the conjugation of reactive 4‐HNE with glutathione to provide a cellular defense against oxidative injury [79,80].…”

Section: Discussionmentioning

confidence: 99%

Differential gene expression in epidermis of mice sensitive and resistant to phorbol ester skin tumor promotion

Riggs

Angel

Abel

et al. 2005

Molecular Carcinogenesis

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Previous data from two-stage carcinogenesis studies in mouse skin demonstrated that genetic control of susceptibility to skin tumor promotion by the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), in crosses between susceptible DBA/2J and resistant C57BL/6J mice is a multigenic trait. Utilizing a cDNA microarray approach, we compared global gene expression profiles in the epidermis of these two mouse strains treated with TPA or vehicle (acetone). Gene expression in the epidermis was analyzed after the treatment to identify global effects of TPA, as well as potential candidate genes that modify susceptibility to skin tumor promotion. DBA/2J and C57BL/6J mice were treated topically four times with 3.4 nmol TPA or acetone over a 2-wk period, and RNA was extracted from epidermis 6 h after the final treatment. Labeled cDNA generated from each group was hybridized to commercial cDNA microarrays (Agilent) containing more than 8000 targets. More than 450 genes were significantly influenced, directly or indirectly, by TPA treatment in the epidermis of either strain. Notably, 44 genes exhibited differential expression between the tumor promotion sensitive and resistant mouse strains. Several genes that were differentially expressed in DBA/2J versus C57BL/6J epidermis after TPA treatment were located in chromosomal regions linked to TPA promotion susceptibility. Three genes, Gsta4, Nmes1 (MGC58382), and Serpinb2, located within promotion susceptibility loci Psl1 (chr 9), Psl2 (chr 2), and Psl3 (chr 1), respectively, were identified in this analysis as potential candidates for modifiers of susceptibility to skin tumor promotion by TPA.

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Section: Discussionmentioning

confidence: 99%

Differential gene expression in epidermis of mice sensitive and resistant to phorbol ester skin tumor promotion

Riggs

Angel

Abel

et al. 2005

Molecular Carcinogenesis

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“…The protein kinase C (PKC) family consists of more than 11 phospholipid-dependent serine/threonine kinases which take part in cellular responses to various agonists, including hormones, some growth factors and neurotransmitters [1, 2, 16, 17, 25]. PKC is abundant in the central nervous system and plays an important role in the regulation of neuronal functions [22, 26].…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane Stimulates MAP Kinase Signal transduction through the Activation of PKC .ALPHA. and .BETA.II in Fetal Rat Cerebral Cortex Cultured Neuron

Hasegawa

Takekoshi

Nagata

et al. 2006

Acta Histochem. Cytochem

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Protein kinase C (PKC) is a key enzyme that participates in various neuronal functions. PKC has also been identified as a target molecule for general anesthetic actions. Raf, mitogen-activated protein kinase (MEK) and extracellular signal-regulated kinase (ERK1/2) have been thought to be target effectors of PKC. In the present study, we attempted to evaluate the effect of sevoflurane on PKC/MAPK cascade signaling in cultured fetal rat cerebral cortex neurons, prepared from embryonic day 18 fetuses. The effects of sevoflurane on the translocation of 7 PKC isoforms (α, βI, βII, γ, δ, ɛ and ζ) were observed by immunoblotting using isoform-selective antibodies to PKCs. The treatment of neurons with sevoflurane induced the translocation of PKC α and PKC βII species from the cytosol to the membrane fraction, which indicated the activation of these PKC isoforms. In contrast, there was no clear change in the distribution of other PKC isoforms. We next examined whether the specific activation of PKC α and βII by sevoflurane could stimulate the MAP kinase signaling pathway in cultured neurons. Raf phosphorylation was increased by the administration of 0.25 mM sevoflurane. The phosphorylation of Raf proteins reached a maximum at 5–10 min. Subsequently, the phosphorylation of MEK proteins was increased at 10–15 min after sevoflurane treatments. That of ERK proteins was induced at 15–60 min. Moreover, the phosphorylation of ERK induced by sevoflurane was significantly decreased by the treatment of PKC inhibitor (staurosporine) and MEK inhibitor (PD98059). On the other hand, the contents of total Raf, MEK and ERK proteins were relatively constant at all times examined. To examine the localization of phosphorylated-ERK protein, immunohistochemical staining of sevoflurane-treated cultured neurons was performed. The phosphorylated-ERK proteins were markedly accumulated in both the cytosol of the cell body and the neurites in the neuronal cells with time after 0.25 mM sevoflurane-treatment. These results demonstrated that sevoflurane induced the phosphorylation of the MAP kinase cascade through the activation of the PKC α and PKC βII species.

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“…In the same way, whether ROS during the pathophysiological state of oxidative stress is capable of activating receptors directly, or if there exist specific cytokines or growth factors that are targeted and their signaling further mediated by ROS, are also matters of further research. Phospholipid metabolites are of high importance as targets for redox signaling, and Takekoshi et al diligently showed that when DAG was oxidized, it activated PKCs more effectively than its non-oxidized counterparts ( Takekoshi et al, 2003 ).…”

Section: Introductionmentioning

confidence: 99%

ROS-Influenced Regulatory Cross-Talk With Wnt Signaling Pathway During Perinatal Development

Chatterjee

Sil

2022

Front. Mol. Biosci.

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Over a century ago, it was found that a rapid burst of oxygen is needed and produced by the sea urchin oocyte to activate fertilization and block polyspermy. Since then, scientific research has taken strides to establish that Reactive Oxygen Species (ROS), besides being toxic effectors of cellular damage and death, also act as molecular messengers in important developmental signaling cascades, thereby modulating them. Wnt signaling pathway is one such developmental pathway, which has significant effects on growth, proliferation, and differentiation of cells at the earliest embryonic stages of an organism, apart from being significant role-players in the instances of cellular transformation and cancer when this tightly-regulated system encounters aberrations. In this review, we discuss more about the Wnt and ROS signaling pathways, how they function, what roles they play overall in animals, and mostly about how these two major signaling systems cross paths and interplay in mediating major cellular signals and executing the predestined changes during the perinatal condition, in a systematic manner.

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Involvement of Lipid Peroxidation in the Alteration of Protein Kinase C Signaling

Cited by 7 publications

References 47 publications

Differential gene expression in epidermis of mice sensitive and resistant to phorbol ester skin tumor promotion

Differential gene expression in epidermis of mice sensitive and resistant to phorbol ester skin tumor promotion

Sevoflurane Stimulates MAP Kinase Signal transduction through the Activation of PKC .ALPHA. and .BETA.II in Fetal Rat Cerebral Cortex Cultured Neuron

ROS-Influenced Regulatory Cross-Talk With Wnt Signaling Pathway During Perinatal Development

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