Evidence map›Paper›PMID 32789724›Full record

ArticleJournal of molecular neuroscience : MN2021

Robust Dopaminergic Differentiation and Enhanced LPS-Induced Neuroinflammatory Response in Serum-Deprived Human SH-SY5Y Cells: Implication for Parkinson's Disease.

Aram Niaz, Jocelyn Karunia, Mawj Mandwie, Kevin A Keay, Giuseppe Musumeci, Ghaith Al-Badri, Alessandro Castorina

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

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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

7 authors at 3 institutions in 2 countries.

Aram NiazLaboratory of Cellular and Molecular Neuroscience (LCMN), School of Life Sciences, Faculty of Science, University of Technology Sydney, PO Box 123, Broadway, NSW, 2007, Australia.
Jocelyn KaruniaLaboratory of Cellular and Molecular Neuroscience (LCMN), School of Life Sciences, Faculty of Science, University of Technology Sydney, PO Box 123, Broadway, NSW, 2007, Australia.
Mawj MandwieLaboratory of Cellular and Molecular Neuroscience (LCMN), School of Life Sciences, Faculty of Science, University of Technology Sydney, PO Box 123, Broadway, NSW, 2007, Australia.
Kevin A KeayLaboratory of Neural Structure and Function (LNSF), School of Medical Sciences, (Anatomy & Histology), Faculty of Medicine and Health, University of Sydney, Sydney, NSW, 2006, Australia.
Giuseppe MusumeciAnatomy, Histology and Movement Sciences Section, Department of Biomedical and Biotechnological Sciences, School of Medicine, University of Catania, via S. Sofia, 87, Catania, 95123, Italy.
Ghaith Al-BadriLaboratory of Cellular and Molecular Neuroscience (LCMN), School of Life Sciences, Faculty of Science, University of Technology Sydney, PO Box 123, Broadway, NSW, 2007, Australia.
Alessandro CastorinaLaboratory of Cellular and Molecular Neuroscience (LCMN), School of Life Sciences, Faculty of Science, University of Technology Sydney, PO Box 123, Broadway, NSW, 2007, Australia. Alessandro.Castorina@UTS.edu.au.ORCID http://orcid.org/0000-0001-7037-759X
University of Technology Sydney · AUThe University of Sydney · AUUniversity of Catania · IT

Funding

University of Technology Sydney Start-up Research Fund 2018
6 · The paper itself

Abstract

Parkinson's disease (PD) is a chronic neurodegenerative condition characterized by motor symptoms such as bradykinesia, resting tremor, and rigidity. PD diagnosis is based on medical history, review of signs, symptoms, neurological and physical examinations. Unfortunately, by the time the disease is diagnosed, dopamine (DA) neuronal loss is often extended, thereby resulting in ineffective therapies. Recent evidence suggests that neuroinflammation may be pivotal during PD onset and progression. However, suitable cellular models and biomarkers to detect early signs of neuroinflammation are still missing. In this study, we developed a well-differentiated DAergic neuronal cell line where we triggered a neuroinflammatory response to assess the temporal expression of the tissue- and urokinase plasminogen activators (tPA and uPA) and their endogenous inhibitor (PAI-1) along with that of pro-inflammatory mediators and the neuronal marker nNOS. Human neuroblastoma cells SH-SY5Y were differentiated into DAergic neuronal-like cells using a combination of 12-O-tetradecanoylphorbol-13-acetate (TPA) and serum depletion. Terminally-differentiated neurons were then exposed to lipopolysaccharide (LPS) for short (up to 24 h) or long term (up to 10 days) to mimic acute or chronic inflammation. Results demonstrated that uPA protein expression was stably upregulated during chronic inflammation, whereas the expression of nNOS protein better reflected the cellular response to acute inflammation. Additional studies revealed that the temporal induction of uPA was associated with increased AKT phosphorylation, but did not seem to involve cAMP-responsive element-binding protein (CREB) activation, nor the mitogen-activated protein kinase (MAPK) pathway. In conclusion, our in vitro data suggests that nNOS and uPA may serve as viable candidate biomarkers of acute and chronic neuroinflammation.

Indexed as

Cell Line, TumorCellular Reprogramming TechniquesCulture Media, Serum-FreeDopaminergic NeuronsHumansLipopolysaccharidesNeurogenesisNitric Oxide Synthase Type IParkinson DiseasePlasminogen Activator Inhibitor 1Proto-Oncogene Proteins c-aktTetradecanoylphorbol AcetateCulture Media, Serum-FreeLipopolysaccharidesNitric Oxide Synthase Type IPlasminogen Activator Inhibitor 1Proto-Oncogene Proteins c-aktTetradecanoylphorbol AcetateAKTDopamineInflammationNeuroblastomaNeurodegenerative diseasesnNOSParkinson’s diseasePlasminogen activatorstPAuPA

Identifiers

PMID32789724
OpenAlexW3049006953

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.