Cited by 61Adenosine and Purinergic SignalingParkinson's Disease Mechanisms and TreatmentsAlzheimer's disease research and treatments

P2X7 receptor-pannexin 1 interaction mediates extracellular alpha-synuclein-induced ATP release in neuroblastoma SH-SY5Y cells

Open access
Wilkaniec, Anna, Gąssowska, Magdalena, Czapski, Grzegorz A., Cieślik, Magdalena, Sulkowski, Grzegorz, Adamczyk, Agata·2017·Purinergic Signalling

Abstract

Abnormalities of alpha-synuclein (ASN), the main component of protein deposits (Lewy bodies), were observed in Parkinson's disease (PD), dementia with Lewy bodies, Alzheimer's disease, and other neurodegenerative disorders. These alterations include increase in the levels of soluble ASN oligomers in the extracellular space. Numerous works have identified several mechanisms of their toxicity, including stimulation of the microglial P2X7 receptor leading to oxidative stress. While the significant role of purinergic signaling-particularly, P2 family receptors-in neurodegenerative disorders is well known, the interaction of extracellular soluble ASN with neuronal purinergic receptors is yet to be studied. Therefore, in this study, we have investigated the effect of ASN on P2 purinergic receptors and ATP-dependent signaling. We used neuroblastoma SH-SY5Y cell line and rat synaptoneurosomes treated with exogenous soluble ASN. The experiments were performed using spectrofluorometric, radiochemical, and immunochemical methods. We found the following: (i) ASN-induced intracellular free calcium mobilization in neuronal cells and nerve endings depends on the activation of purinergic P2X7 receptors; (ii) activation of P2X7 receptors leads to pannexin 1 recruitment to form an active complex responsible for ATP release; and (iii) ASN greatly decreases the activity of extracellular ecto-ATPase responsible for ATP degradation. Thus, it is concluded that purinergic receptors might be putative pharmacological targets in the molecular mechanism of extracellular ASN toxicity. Interference with P2X7 signaling seems to be a promising strategy for the prevention or therapy of PD and other neurodegenerative disorders.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1007/s11302-017-9567-2

Cites

104 of 104 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • α-synuclein induces mitochondrial dysfunction and microglial activation caused by P2X7 receptor stimulation.

    “Although these symptoms might not be disease-related, studies show that α-synuclein induces mitochondrial dysfunction and microglial activation caused by P2X7 receptor stimulation [143, 144].”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Wilkaniec, A., Gąssowska, M., Czapski, G. A., Cieślik, M., Sulkowski, G., & Adamczyk, A.
Affiliations
Mossakowski Medical Research Institute, Polish Academy of Sciences (PL)
Corresponding author
Wilkaniec, Anna
Venue
Purinergic Signalling
Published
2017-05-17
Volume
13
Issue
3
Pages
347-361
ISSN
  • 1573-9538 (ISSN-L)
  • 1573-9546
OpenAlex
W2614544395
Cited by
61
References
104
Citations by year
2026: 6 · 2025: 7 · 2024: 6 · 2023: 3 · 2022: 10 · 2021: 7 · 2020: 9 · 2019: 4 · 2018: 8 · 2017: 1
FWCI
4.61
Type
journal article
Language
en
Open access
Locations
  • Purinergic Signalling (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
Narodowe Centrum Nauki (PL) (2013/09/D/NZ3/0135)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Adenosine and Purinergic Signaling
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Keywords
alpha-synuclein, P2X7 receptor, pannexin 1, ATP release, purinergic signaling, calcium mobilization, ecto-ATPase, neurodegenerative diseases, Parkinson's disease, Lewy bodies, SH-SY5Y cells, synaptoneurosomes
MeSH terms
Adenosine Triphosphate, Animals, Calcium, Extracellular Space, Humans, Male, Nerve Tissue Proteins, Rats, Wistar, Microglia, Connexins, Cell Line, Tumor, alpha-Synuclein, Receptors, Purinergic P2X7

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review