Neuroprotection by fructose-1,6-bisphosphate involves ROS alterations via p38 MAPK/ERK

Park, Jee-Young; Kim, Eun Joo; Kwon, Kyoung Ja; Moon, Chang-Hyun; Lee, Soo Hwan; Baik, Eun Joo

doi:10.1016/j.brainres.2004.08.039

Cited by 38 publications

(37 citation statements)

References 47 publications

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“…A similar sequence of events was also suggested for the involvement of H 2 O 2 in cytokine gene expression and apoptosis [22,23] . Other studies in both animal models and human neutrophils [24,25] have, on the other hand, reported an ERK1/2-dependent activation of NADPH oxidase, in agreement with our present results. These conflicting observations may be explained by cellspecific differences in the signaling pathways commonly observed across cell types.…”

Section: Discussionsupporting

confidence: 83%

“…There is conflicting data in the literature concerning the hierarchical relationship between ERK1/2 phosphorylation and ROS generation in signaling mechanisms [10,[22][23][24][25]. The study of Greene et al [10] on H 2 O 2 -mediated signaling in 5HT-activated rat mesangial cells, have situated ERK1/2 activation downstream of NADPH oxidase activation.…”

Section: Discussionmentioning

confidence: 95%

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Protein Kinase C- and Reactive Oxygen Species-Dependent Stimulation of Intracellular cAMP in Human Eosinophils

Ezeamuzie¹,

Taslim²

2008

Med Princ Pract

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Objective: The objective of this study was to investigate the role of the extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) in the signalling pathway of the novel protein kinase C (PKC)- and reactive oxygen species (ROS)-dependent stimulation of intracellular adenosine 3′,5′-cyclic monophosphate (cAMP) production in human eosinophils. Materials and Methods: Immunomagnetically purified human eosinophils were stimulated in vitro with a PKC activator, phorbol myristate acetate (PMA), and the cAMP response in the presence of a phosphodiesterase inhibitor, rolipram, was determined. The role of ERK1/2 phosphorylation was investigated using specific inhibitors and Western blot analysis. Results: The PMA-stimulated eosinophils responded with a profound increase in intracellular levels of cAMP that was dependent on both PKC and ROS, as confirmed by the use of specific inhibitors: Ro 31-8220 for PKC and diphenyleneiodonium (DPI) for the ROS-generating enzyme NADPH oxidase. Pre-treatment of cells with the ERK1/2 inhibitor PD 98059, but not the p38-MAPK inhibitor SB203580, nor the PI3 kinase inhibitor, wortmannin, abolished the response. PMA treatment induced the phosphorylation of ERK1/2 with a time course that is consistent with a role in the cAMP response. The ERK1/2 phosphorylation was abolished by the ERK1/2 inhibitor PD 98059 and the PKC inhibitor Ro 31-8220, but not the NADPH oxidase inhibitor DPI. Conclusion: These results reveal the involvement of ERK1/2 in the signalling mechanism of PMA-stimulated, PKC- and ROS-dependent stimulation of cAMP production in human eosinophils, and show that ERK1/2 phosphorylation is upstream of ROS production in the signalling pathway.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 95%

Protein Kinase C- and Reactive Oxygen Species-Dependent Stimulation of Intracellular cAMP in Human Eosinophils

Ezeamuzie¹,

Taslim²

2008

Med Princ Pract

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“…These findings are consistent with the previous reports that other ROCK inhibitors, such as fasudil and H1152, suppressed stress-activated MAPK family members (p38 and c-Jun Nterminal kinase [JNK]). [53][54][55] The inhibition of p38 has been shown to be potentially beneficial in experimental nerve trauma, excitotoxicity, 56 and growth factor withdrawal. 57 As a result, p38 inhibitors have recently been claimed as novel and potential therapeutics for neurodegenerative diseases.…”

Section: Discussionmentioning

confidence: 99%

Topical Ripasudil Suppresses Retinal Ganglion Cell Death in a Mouse Model of Normal Tension Glaucoma

Akaiwa

Namekata

Azuchi

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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METHODS. Topical administration (5 lL/day) of two different concentrations of ripasudil (0.4% and 2%) were applied to EAAC1 KO mice from 5 to 12 weeks old. Optical coherence tomography, multifocal electroretinograms, the measurement of intraocular pressure (IOP), and histopathology analyses were performed at 5, 8, and 12 weeks old. Retrograde labeling of retinal ganglion cells (RGCs), immunoblot, and immunohistochemical analyses of phosphorylated p38 mitogen-activated protein kinase (MAPK) in the retina were performed at 8 weeks old.RESULTS. Topical ripasudil ameliorated retinal degeneration and improved visual function in EAAC1 KO mice at both 8 and 12 weeks old. Ripasudil reduced IOP and strongly suppressed the phosphorylation of p38 MAPK that stimulates RGC death in EAAC1 KO mice.CONCLUSIONS. These results suggest that, in addition to IOP reduction, ripasudil prevents glaucomatous retinal degeneration by neuroprotection, which is achieved by suppressing celldeath signaling pathways.

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“…Additionally, PKC, cPLA 2 and p38 MAPK may serve as the up-and downstream signals of ROS, since ROS not only directly activate PKC and MAPKs, but also directly activated by PKC, cPLA 2 and p38 MAPK. [30][31][32][33][34] On the basis of our observation, we hypothesized that PPARδ-induced ROS stimulated signal cascades such as PKC, cPLA 2 and p38 MAPK, and ROS amplification. These responses eventually contribute to mouse ES cells proliferation.…”

Section: Discussionmentioning

confidence: 90%

PPARδ agonist-mediated ROS stimulates mouse embryonic stem cell proliferation through cooperation of p38 MAPK and Wnt/β-catenin

Jeong

Lee²,

Lee³

et al. 2009

Cell Cycle

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N O T D I S T R I B U T E .PPARδ (peroxisome proliferator-activated receptor delta) is a member of the nuclear receptor superfamily. However, its function in tissues and cells is unknown, particularly as related to stem cell biology. We therefore investigated the PPARδ effects on DNA synthesis in mouse embryonic stem cells (ES cells) and its related signal pathways. PPARδ increased biphasic reactive oxygen species (ROS) production at 15 min and at 120 min incubation. PPARδ significantly increased [ 3 H] thymidine incorporation levels at various concentrations (10 -8 M to 10 -6 M) and incubation times (12 to 48 hr), and this activity was blocked by antioxidants. In addition, PPARδ increased protein kinase C (PKC), cytosolic phospholipase A 2 (cPLA 2 ) and p38 mitogen-activated protein kinase (p38 MAPK) phosphorylation, and Wnt/β-catenin activation. PPARδ increased the protein levels of cell cycle regulators, and these levels were abolished by antioxidants, bisindolymaleimide I, SB203580 and β-catenin specific siRNA. In addition, the effect of PPARδ on increased [ 3 H] thymidine incorporation was blocked by bisindolymaleimide I, SB203580 and β-catenin specific siRNA. In conclusion, PPARδ agonist enhanced mouse ES cells proliferation through ROS-mediated p38 MAPK and Wnt/β-catenin activation.

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Neuroprotection by fructose-1,6-bisphosphate involves ROS alterations via p38 MAPK/ERK

Cited by 38 publications

References 47 publications

Protein Kinase C- and Reactive Oxygen Species-Dependent Stimulation of Intracellular cAMP in Human Eosinophils

Protein Kinase C- and Reactive Oxygen Species-Dependent Stimulation of Intracellular cAMP in Human Eosinophils

Topical Ripasudil Suppresses Retinal Ganglion Cell Death in a Mouse Model of Normal Tension Glaucoma

PPARδ agonist-mediated ROS stimulates mouse embryonic stem cell proliferation through cooperation of p38 MAPK and Wnt/β-catenin

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