Interaction Among Mitochondria, Mitogen‐Activated Protein Kinases, and Nuclear Factor‐κB in Cellular Models of Parkinson's Disease

Cassarino, David S.; Em, Halvorsen; Rh, Swerdlow; Nn, Abramova; Wd, Parker; Tw, Sturgill; Jp, Bennett

doi:10.1046/j.1471-4159.2000.0741384.x

Cited by 115 publications

(67 citation statements)

References 48 publications

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“…Therefore, the site of action involved in the neuronal protection of meloxicam is most likely to be at the upstream signaling cascade prior to the mitochondria in the MPP + -induced neuronal death. The recently established two pro-apoptotic molecules, p38 MAP kinase and c-Jun N-terminal kinase (JNK), are rapidly activated (Cassarino et al, 2000) before the mitochondrial collapse (Fall and Bennett, 1999) when SH-SY5Y cells are exposed to MPP + .…”

Section: Discussionmentioning

confidence: 99%

Meloxicam protects cell damage from 1-methyl-4-phenyl pyridinium toxicity via the phosphatidylinositol 3-kinase/Akt pathway in human dopaminergic neuroblastoma SH-SY5Y cells

et al. 2010

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Parkinson's disease (PD) is a common neurodegenerative disorder characterized by dopaminergic neuronal death in the substantia nigra pars compacta. There is growing interest in the effects of nonsteroidal antiinflammatory drugs (NSAIDs) against PD progression. In this study, we investigated the neuroprotective effect of NSAIDs on neuronal damage induced by 1-methyl-4-phenyl pyridinium (MPP + ) in human

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Section: Discussionmentioning

confidence: 99%

Meloxicam protects cell damage from 1-methyl-4-phenyl pyridinium toxicity via the phosphatidylinositol 3-kinase/Akt pathway in human dopaminergic neuroblastoma SH-SY5Y cells

et al. 2010

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“…Thus, flavonoids might be able to modulate mitochondrial functions by binding to ATP binding sits on the ANT, ATPases or others. Indeed, bongkrekic acid an antagonist of the ATP-binding site of the ANT has been shown to prevent mPT and the early activation of JNK in MPP + -induced neuronal injury as a model for Parkinson's disease [28].…”

Section: Flavonoids: Neuroprotective Agents In Vivo and In Vitro?mentioning

confidence: 99%

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

Schroeter

Boyd

Spencer

et al. 2002

Neurobiology of Aging

310

178

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Oxidative and nitrosative stress is increasingly associated with the pathology of neurodegeneration and aging. The molecular mechanisms underlying oxidative/nitrosative stress-induced neuronal damage are emerging and appear to involve a mode of death in which mitogen-activated protein kinase (MAPK) signaling pathways are strongly implicated. Thus, attention is turning towards the modulation of intracellular signaling as a therapeutic approach against neurodegeneration. Both endogenous and dietary agents have been suggested as potent modulators of intracellular signal transduction, e.g. nitric oxide and flavonoids, respectively. This review addresses recent findings on the biological effects of flavonoids and nitric oxide in neurodegeneration and aims to elucidate the rationale for their prospective use as modulators of cellular signal transduction. © 2002 Elsevier Science Inc. All rights reserved.Keywords: Apoptosis; Oxidative stress; Neuron; Flavonoids; MAP kinase; JNK; ERK; Epicatechin; Nitric oxide; Mitochondria; Redox status; Polyphenols Abbreviations: AKT, serine/threonine kinase (also known as protein kinase B); AP-1, activator protein-1; Apaf-1, apoptosis protease activating factor-1; ASK1, apoptosis signal-regulating kinase-1; Bad, Bcl-2/BclX Lassociated death promoting protein; Bax, pro-apoptotic protein of the Bcl-2 family; Bcl-2, B-cell lymphoma 2: protein with anti-apoptotic properties; BclX L , long form of Bclx: anti-apoptotic protein of the Bcl-2 family; Caspase, cysteinyl aspartic acid-protease; c-Jun, mammalian equivalent of Jun: part of the AP-1 transcription complex; CREB, cAMP response element binding protein; DIABLO/smac, mitochondria-related pro-apoptotic protein: inhibits XIAP; ERK1/2, extracellular signal-related kinase; Fas, CD95: member of the TNF receptor family; GSHST, glutathione Stransferase; JNK, c-Jun amino-terminal kinase; MAPK, mitogen-activated protein kinase; MAPKK, MAPK kinase; MAPKKK, MAPKK kinase; MEK1/2, ERK1/2-specific MAPKK; MKK4/7, JNK-specific MAPKK; MSK1, mitogen-and stress-activated kinase-1; NF-B, nuclear factor of immunoglobulin k locus in B-cells; ONOO − , peroxynitrite anion; p53, pro-apoptotic tumor suppressor gene product; PI3-kinase, phosphoinositol 3-kinase; Ras, small G-protein; RNS, reactive nitrogen species; ROS, reactive oxygen species; RSK, pp90 ribosomal S6 kinase; SAPK, stressactivated protein kinase; XIAP, X-linked inhibitor of apoptosis: inhibits the activation of caspase-9

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“…Stress-activated protein kinases, such as, JNK and p38 are known potent effectors of neuronal apoptosis in response to various stimuli (Mielke and Herdegen, 2000). In fact, the active forms of JNK and p38 have been found in the PD brain post-mortem (Ferrer et al, 2001) as well as in experimental animals (Saporito et al, 1999(Saporito et al, , 2000 and in culture models of PD (Cassarino et al, 2000;Choi et al, 2004). Furthermore, it has been reported that the 6-OHDA-induced phosphorylation of p38 is linked to the activations of caspase-8 and -9, and thus, to apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of fustin, a flavonoid from Rhus verniciflua Stokes, on 6-hydroxydopamine-induced neuronal cell death

Park

Lee²,

Park³

et al. 2007

Exp Mol Med

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Abstract6-Hydroxydopamine (6-OHDA) is a neurotoxin and is commonly used to generate experimental models of Parkinson's disease (PD). In this study, we investigated the signaling molecules involved in the 6-OHDA-induced cell death using a neuronal catecholaminergic cell line (SK-N-SH cells), and the protective effect of fustin, a flavonoid from Rhus verniciflua Stokes, on 6-OHDA-induced neuronal death. 6-OHDA significantly increased levels of reactive oxygen species (ROS), intracellular Ca 2+ ([Ca 2+ ] i ), and p38 phosphorylation. In addition, this ROS increase by 6-OHDA was reduced by pretreatment with N-acetylcysteine (NAC), a free radical scavenger, but not by bis-(o-aminophenoxy)-ethane-N,N,N,Ntetraacetic acid (BAPTA), a Ca 2+ chelator. However, the [Ca 2+ ] i increase induced by 6-OHDA was suppressed by NAC. Moreover, pretreatment with NAC or BAPTA significantly prevented the 6-OHDAinduced increases in p38 phosphorylation, Bax/ Bcl-2 ratio, and caspase-3 activity. Although 6-OHDA-increased phosphorylation of p38 was prevented by NAC or BAPTA, inhibition of p38 by SB203580 did not suppress ROS, Bax/Bcl-2 ratio, or caspase-3 activity increases, and only partially prevented 6-OHDA-induced cell death, thus demonstrating that p38 activation is a component of a signaling pathway leading to the initiation of 6-OHDA-induced cell death, which acts in parallel with an ROS-Ca 2+ -Bcl-2-caspase-3 pathway. Moreover, fustin not only suppressed 6-OHDA-induced cell death in a concentration-dependent manner but also blocked 6-OHDA-induced increases in ROS, [Ca 2+ ] i , Bax/Bcl-2 ratio, caspase-3 activity, and p38 phosphorylation. These results suggest that fustin exerts neuroprotection against 6-OHDA-induced cell death.

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Interaction Among Mitochondria, Mitogen‐Activated Protein Kinases, and Nuclear Factor‐κB in Cellular Models of Parkinson's Disease

Abstract: Abstract:Oxidative stress induced by acute complex

Cited by 115 publications

References 48 publications

Meloxicam protects cell damage from 1-methyl-4-phenyl pyridinium toxicity via the phosphatidylinositol 3-kinase/Akt pathway in human dopaminergic neuroblastoma SH-SY5Y cells

Meloxicam protects cell damage from 1-methyl-4-phenyl pyridinium toxicity via the phosphatidylinositol 3-kinase/Akt pathway in human dopaminergic neuroblastoma SH-SY5Y cells

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

Protective effects of fustin, a flavonoid from Rhus verniciflua Stokes, on 6-hydroxydopamine-induced neuronal cell death

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