Over-expression of map kinase phosphatase-1 (MKP-1) suppresses neuronal death through regulating JNK signaling in hypoxia/re-oxygenation

Koga, Shunsuke; Kojima, Shunsuke; Kishimoto, Takashi; Kuwabara, Satoshi; Yamaguchi, Atsushi

doi:10.1016/j.brainres.2011.12.004

Cited by 38 publications

(25 citation statements)

References 46 publications

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“…It has recently been reported that MAPK phosphatase-1 (a DUSP family member) is upregulated in the rat after MCA occlusion and that conditional overexpression of MAPK phosphatase-1 suppressed phosphorylation of JNK as well as cell death in neuroblastoma cells subjected to hypoxia reoxygenation. 32 Our results corroborate these findings of an association between DUSP8 and JNK.…”

Section: Discussionsupporting

confidence: 89%

Prevention of JNK Phosphorylation as a Mechanism for Rosiglitazone in Neuroprotection after Transient Cerebral Ischemia: Activation of Dual Specificity Phosphatase

Okami

Narasimhan

Yoshioka

et al. 2012

J Cereb Blood Flow Metab

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Rosiglitazone, a synthetic peroxisome proliferator-activated receptor-g (PPARg) agonist, prevents cell death after cerebral ischemia in animal models, but the underlying mechanism has not been clarified. In this study, we examined how rosiglitazone protects neurons against ischemia. Mice treated with rosiglitazone were subjected to 60 minutes of focal ischemia followed by reperfusion. Rosiglitazone reduced infarct volume after ischemia and reperfusion. We show that this neuroprotective effect was reversed with a PPARg antagonist. Western blot analysis showed a significant increase in expression of phosphorylated stress-activated protein kinases (c-Jun N-terminal kinase (JNK) and p38) in ischemic brain tissue. Rosiglitazone blocked this increase. Furthermore, we observed that rosiglitazone increased expression of the dual-specificity phosphatase 8 (DUSP8) protein and messenger RNA in ischemic brain tissue. Dual-specificity phosphatase 8 is a mitogen-activated protein kinase phosphatase that can dephosphorylate JNK and p38. Another key finding of the present study was that knockdown of DUSP8 in primary cultured cortical neurons that were subjected to oxygen-glucose deprivation diminished rosiglitazone's effect on downregulation of JNK phosphorylation. Thus, rosiglitazone's neuroprotective effect after ischemia is mediated by blocking JNK phosphorylation induced by ischemia via DUSP8 upregulation.

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Section: Discussionsupporting

confidence: 89%

Prevention of JNK Phosphorylation as a Mechanism for Rosiglitazone in Neuroprotection after Transient Cerebral Ischemia: Activation of Dual Specificity Phosphatase

Okami

Narasimhan

Yoshioka

et al. 2012

J Cereb Blood Flow Metab

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“…This maybe due to the cytokine-dependent induction, in parallel with NMI, of other JNK regulators. Our RNA sequencing data of cytokine-treated human islet cells (30) support this hypothesis, showing a significant up-regulation of several phosphatases such DUSP1 (65) and DUSP16 (66,67) in IL-1␤ ϩ IFN-␥-treated islets.…”

Section: Discussionsupporting

confidence: 71%

A Combined “Omics” Approach Identifies N-Myc Interactor as a Novel Cytokine-induced Regulator of IRE1α Protein and c-Jun N-terminal Kinase in Pancreatic Beta Cells

Brozzi

Gerlo

Grieco

et al. 2014

Journal of Biological Chemistry

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Background: Cytokine-induced IRE1␣ activation regulates adaptive/pro-apoptotic endoplasmic reticulum (ER) stress transition in type 1 diabetes (T1D). Results: The IRE1␣-binding protein NMI modulates JNK activation and apoptosis in beta cells. Conclusion: NMI induction is a novel negative feedback mechanism regulating ER stress and apoptosis in cytokine-exposed beta cells. Significance: Clarifying cytokine modulation of ER stress may provide information to protect beta cells in early T1D.

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“…It is also tempting to speculate that Mkp1 may be up-regulated in both SN dopaminergic neurons and microglia in an attempt at cellular neuroprotection following exposure to 6-OHDA. Indeed, strategies that increase Mkp1 in the central nervous system (CNS) have been shown to be neuroprotective in a number of animal models of neurodegenerative and inflammatory CNS insults (Eljaschewitsch et al 2006; Koga et al 2012; Taylor et al 2013). …”

Section: Discussionmentioning

confidence: 99%

“…Mitogen-activated protein kinase phosphatases (MKPs) provide a negative feedback mechanism for regulating MAPK activity (including p38, JNK and ERK) by de-phosphorylating these kinases (Farooq and Zhou 2004). Mkp1 has also been shown to offer neuroprotection in models of Huntington’s disease (HD) (Taylor et al 2013), and to prevent neuronal death in a model of acute cerebral infarction (Koga et al 2012). In light of these findings, the aim of the present study was to assess Mkp1 expression in the striatum and midbrain in the 6-OHDA MFB model and the four-site 6-OHDA striatal lesion models of PD.…”

Section: Introductionmentioning

confidence: 99%

Expression of endogenous Mkp1 in 6-OHDA rat models of Parkinson’s disease

et al. 2014

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We have previously demonstrated that mitogen-activated protein kinase phosphatase 1, Mkp1, is expressed in the developing and rat adult substantia nigra and striatum, where it promotes the growth of nigral dopaminergic neurons. Mkp1 may therefore have therapeutic potential for Parkinson’s disease. In the present study, we have assessed the expression of Mkp1 and TH in the substantia nigra and striatum of parkinsonian rat models. Expression was measured at 4 and 10 days post-lesion in the 6-hydroxydopamine (6-OHDA) medial forebrain bundle lesion model and after 4, 10 and 28 days in the 6-OHDA striatal lesion model. Our results show that Mkp1 expression was transiently up-regulated in the substantia nigra at 4 days post-6-OHDA administration in the two models while TH expression was decreased at the later time-points examined. These data suggest that Mkp1 may play a role in counteracting the neurotoxic effects of 6-OHDA in nigral dopaminergic neurons.

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Over-expression of map kinase phosphatase-1 (MKP-1) suppresses neuronal death through regulating JNK signaling in hypoxia/re-oxygenation

Cited by 38 publications

References 46 publications

Prevention of JNK Phosphorylation as a Mechanism for Rosiglitazone in Neuroprotection after Transient Cerebral Ischemia: Activation of Dual Specificity Phosphatase

Prevention of JNK Phosphorylation as a Mechanism for Rosiglitazone in Neuroprotection after Transient Cerebral Ischemia: Activation of Dual Specificity Phosphatase

A Combined “Omics” Approach Identifies N-Myc Interactor as a Novel Cytokine-induced Regulator of IRE1α Protein and c-Jun N-terminal Kinase in Pancreatic Beta Cells

Expression of endogenous Mkp1 in 6-OHDA rat models of Parkinson’s disease

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