Evidence map›Paper›PMID 25976369›Full record

ArticleMolecular neurobiology2016

Neuroprotective Effect of JZL184 in MPP(+)-Treated SH-SY5Y Cells Through CB2 Receptors.

María S Aymerich, Estefanía Rojo-Bustamante, Carmen Molina, Marta Celorrio, Juan A Sánchez-Arias, Rafael Franco

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In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.7field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 44 citations in OpenAlex.

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  10. The endocannabinoidome mediatorFrontiers in aging neuroscience · 2022
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

María S AymerichDepartment of Biochemistry and Genetics, School of Science, University of Navarra, Pamplona, 31008, Spain. maymerich@unav.es.
Estefanía Rojo-BustamanteDepartment of Biochemistry and Genetics, School of Science, University of Navarra, Pamplona, 31008, Spain.
Carmen MolinaProgram of Neurosciences, Center for Applied Medical Research (CIMA), University of Navarra, Pío XII 55, 31008, Pamplona, Spain.
Marta CelorrioProgram of Neurosciences, Center for Applied Medical Research (CIMA), University of Navarra, Pío XII 55, 31008, Pamplona, Spain.
Juan A Sánchez-AriasSmall Molecules Group, Center for Applied Medical Research (CIMA), University of Navarra, 31008, Pamplona, Spain.
Rafael FrancoProgram of Neurosciences, Center for Applied Medical Research (CIMA), University of Navarra, Pío XII 55, 31008, Pamplona, Spain.
Universidad de Navarra · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growing evidence suggests that the endocannabinoid system plays a role in neuroprotection in Parkinson's disease. Recently, we have shown the neuroprotective effect of monoacylglycerol lipase (MAGL) inhibition with JZL184 in the chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model. However, further investigation is needed to determine the neuroprotective mechanisms of the endocannabinoid system on the nigrostriatal pathway. The aim of this work was to investigate whether the neuroprotective effect of JZL184 in mice could be extended to an in vitro cellular model to further understand the mechanism of action of the drug. The SH-SY5Y cell line was selected based on its dopaminergic-like phenotype and its susceptibility to 1-methyl-4-phenylpyridinium iodide (MPP(+)) toxicity. Furthermore, SH-SY5Y cells express both cannabinoid receptors, CB1 and CB2. The present study describes the neuroprotective effect of MAGL inhibition with JZL184 in SH-SY5Y cells treated with MPP(+). The effect of JZL184 in cell survival was blocked by AM630, a CB2 receptor antagonist, and it was mimicked with JWH133, a CB2 receptor agonist. Rimonabant, a CB1 receptor antagonist, did not affect JZL184-induced cell survival. These results demonstrate that the neuroprotective effect of MAGL inhibition with JZL184 described in animal models of Parkinson's disease could be extended to in vitro models such as SH-SY5Y cells treated with MPP(+). This represents a useful tool to study mechanisms of neuroprotection mediated by MAGL inhibition, and we provide evidence for the possible involvement of CB2 receptors in the improvement of cell survival.

Indexed as

1-Methyl-4-phenylpyridiniumAmidohydrolasesBenzodioxolesCell Line, TumorEnzyme InhibitorsFatty Acid Amide HydrolasesHumansMonoacylglycerol LipasesNeuroprotective AgentsNeurotoxinsPiperidinesReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB21-Methyl-4-phenylpyridiniumAmidohydrolasesBenzodioxolesEnzyme InhibitorsFatty Acid Amide HydrolasesJZL 184Monoacylglycerol LipasesNeuroprotective AgentsNeurotoxinsPiperidinesReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB22-AGCannabinoid receptorEndocannabinoidJZL184Monoacylglycerol lipaseNeuroprotection

Identifiers

PMID25976369
OpenAlexW236671428

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.