Evidence mapPaperPMID 27366949Full record

ArticleOncotarget2016

Delta-9-tetrahydrocannabinol protects against MPP+ toxicity in SH-SY5Y cells by restoring proteins involved in mitochondrial biogenesis.

Marie-Louise Zeissler, Jordan Eastwood, Kieran McCorry, C Oliver Hanemann, John P Zajicek, Camille B Carroll

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. The endocannabinoidome mediatorFrontiers in aging neuroscience · 2022
    Article
  8. Review
  9. Review
  10. Review
  11. Identification of the Ghrelin and Cannabinoid CBInternational journal of molecular sciences · 2021
    Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Modified level of miR-376a is associated with Parkinson's disease.Journal of cellular and molecular medicine · 2020
    Article
  19. Review
  20. Review
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 2 institutions in 1 country.

Marie-Louise ZeisslerPlymouth University Peninsula Schools of Medicine and Dentistry, Plymouth, PL6 8BU, United Kingdom.
Jordan EastwoodPlymouth University Peninsula Schools of Medicine and Dentistry, Plymouth, PL6 8BU, United Kingdom.
Kieran McCorryPlymouth University Peninsula Schools of Medicine and Dentistry, Plymouth, PL6 8BU, United Kingdom.
C Oliver HanemannPlymouth University Peninsula Schools of Medicine and Dentistry, Plymouth, PL6 8BU, United Kingdom.
John P ZajicekSchool of Medicine, Medical and Biological Sciences, University of St Andrews, North Haugh, St Andrews, KY16 9TF, United Kingdom.
Camille B CarrollPlymouth University Peninsula Schools of Medicine and Dentistry, Plymouth, PL6 8BX, United Kingdom.
Peninsula College of Medicine and Dentistry · GBUniversity of St Andrews · GB

Funding

Medical Research Council G0501542
6 · The paper itself

Abstract

Proliferator-activated receptor γ (PPARγ) activation can result in transcription of proteins involved in oxidative stress defence and mitochondrial biogenesis which could rescue mitochondrial dysfunction in Parkinson's disease (PD).The PPARγ agonist pioglitazone is protective in models of PD; however side effects have limited its clinical use. The cannabinoid Δ9-tetrahydrocannabinol (Δ9-THC) may have PPARγ dependent anti-oxidant properties. Here we investigate the effects of Δ9-THC and pioglitazone on mitochondrial biogenesis and oxidative stress. Differentiated SH-SY5Y neuroblastoma cells were exposed to the PD relevant mitochondrial complex 1 inhibitor 1-methyl-4-phenylpyridinium iodide (MPP+). We found that only Δ9-THC was able to restore mitochondrial content in MPP+ treated SH-SY5Y cells in a PPARγ dependent manner by increasing expression of the PPARγ co-activator 1α (PGC-1α), the mitochondrial transcription factor (TFAM) as well as mitochondrial DNA content. Co-application of Δ9-THC with pioglitazone further increased the neuroprotection against MPP+ toxicity as compared to pioglitazone treatment alone. Furthermore, using lentiviral knock down of the PPARγ receptor we showed that, unlike pioglitazone, Δ9-THC resulted in a PPARγ dependent reduction of MPP+ induced oxidative stress. We therefore suggest that, in contrast to pioglitazone, Δ9-THC mediates neuroprotection via PPARγ-dependent restoration of mitochondrial content which may be beneficial for PD treatment.

Indexed as

1-Methyl-4-phenylpyridiniumCell Line, TumorDronabinolHumansMitochondriaMitochondrial DiseasesNeuroblastomaNeuroprotective AgentsOxidative StressParkinson DiseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPioglitazonePPAR gammaThiazolidinediones1-Methyl-4-phenylpyridiniumDronabinolNeuroprotective AgentsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPioglitazonePPAR gammaPPARGC1A protein, humanThiazolidinedionesmitochondrial biogenesisMPP+Parkinson’s diseaseperoxisome proliferator-activated receptorΔ9-tetrahydrocannabinol

Identifiers

PMID27366949
PMCPMC5216821
OpenAlexW2470961493

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.