Evidence map›Paper›PMID 24740430›Full record

ArticleNeurotoxicity research2014

PACAP protects against inflammatory-mediated toxicity in dopaminergic SH-SY5Y cells: implication for Parkinson's disease.

Dwayne Brown, Andrea Tamas, Dora Reglodi, Yousef Tizabi

Abstract read
PubMed Publisher
In one paragraph

Article in Neurotoxicity research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-weighted citation impact, top 19% 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

26 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. The role of amphipathic and cationic helical peptides in Parkinson's disease.Protein science : a publication of the Protein Society · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Effects of Pituitary Adenylate Cyclase Activating Polypeptide on Cell Death.International journal of molecular sciences · 2022
    Review
  7. Review
  8. Article
  9. Article
  10. The Emerging Role of Neuropeptides in Parkinson's Disease.Frontiers in aging neuroscience · 2021
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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

4 authors at 2 institutions in 2 countries.

Dwayne BrownDepartment of Pharmacology, Howard University College of Medicine, 520 W Street NW, Washington, DC, 20059, USA.
Andrea Tamas
Dora Reglodi
Yousef Tizabi
Howard University · USUniversity of Pecs · HU

Funding

The Howard University SCORE Program Supplemental GrantS06GM008016 · NIGMS · HOWARD UNIVERSITY · PI LITTLETON, GEORGE K · 1989 to 2009
$16.1M
NIGMS NIH HHS 2 SO6 GM08016-39
6 · The paper itself

Abstract

There has been a growing recognition of the role of neuroinflammation caused by microglia-exaggerated release of inflammatory mediators in the pathogenesis of Parkinson's disease (PD). Pituitary adenylate cyclase activating polypeptide (PACAP) is an endogenous 38 amino acid containing neuropeptide that has been shown to possess neurotrophic as well as neuroprotective properties. In this study, we sought to determine whether PACAP could protect SH-SY5Y dopaminergic cells against toxicity induced by inflammatory mediators. For this purpose, THP-1 cells which possess microglia-like property were stimulated by a combination of lipopolysaccharide (LPS) and interferon gamma (IFN-γ), and the media containing inflammatory mediators were isolated and applied to SH-SY5Y cells. Such treatment resulted in approximately 54 % cell death as well as a reduction in brain-derived neurotrophic factor (BDNF) and phosphorylated cyclic AMP response element-binding protein (p-CREB). Pretreatment of the SH-SY5Y cells with PACAP (1-38) dose-dependently attenuated toxicity induced by the inflammatory mediators. PACAP effects, in turn, were dose-dependently blocked by the PACAP receptor antagonist (PACAP 6-38). These results suggest protective effects of PACAP against inflammatory-induced toxicity in a cellular model of PD that is likely mediated by enhancement of cell survival markers through activation of PACAP receptors. Hence, PACAP or its agonists could be of therapeutic benefit in inflammatory-mediated PD.

Indexed as

ApoptosisBrain-Derived Neurotrophic FactorCaspase 3Cell Line, TumorCell SurvivalCyclic AMP Response Element-Binding ProteinDopaminergic NeuronsEncephalitisHumansInterferon-gammaLipopolysaccharidesParkinson DiseasePeptide FragmentsPhosphorylationPituitary Adenylate Cyclase-Activating PolypeptideADCYAP1 protein, humanBrain-Derived Neurotrophic FactorCaspase 3Cyclic AMP Response Element-Binding ProteinInterferon-gammaLipopolysaccharidesPeptide Fragmentspituitary adenylate-cyclase-activating-peptide (6-38)Pituitary Adenylate Cyclase-Activating Polypeptide

Identifiers

PMID24740430
OpenAlexW2043011979

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.