Evidence map›Paper›PMID 35222364›Full record

ArticleFrontiers in immunology2022

P2X7 Receptor Triggers Lysosomal Leakage Through Calcium Mobilization in a Mechanism Dependent on Pannexin-1 Hemichannels.

Stephanie Alexia Cristina Silva Santos, Pedro Muanis Persechini, Bianca Monteiro Henriques-Santos, Victória Gabriela Bello-Santos, Newton G Castro, Júlia Costa de Sousa, Fernando Ariel Genta, Marcelo Felippe Santiago, Robson Coutinho-Silva, Luiz Eduardo Baggio Savio and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 14 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

11 authors at 3 institutions in 1 country.

Stephanie Alexia Cristina Silva SantosLaboratory of Molecular Biology and Biochemistry of Proteins, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Pedro Muanis PersechiniLaboratory of Immuno-Biophysics, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Bianca Monteiro Henriques-SantosLaboratory of Insect Physiology and Biochemistry, Oswaldo Cruz Institute - Oswaldo Cruz Foundation (IOC-FIOCRUZ), Rio de Janeiro, Brazil.
Victória Gabriela Bello-SantosLaboratory of Molecular Pharmacology, Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Newton G CastroLaboratory of Molecular Pharmacology, Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Júlia Costa de SousaLaboratory of Molecular Biology and Biochemistry of Proteins, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Fernando Ariel GentaLaboratory of Insect Physiology and Biochemistry, Oswaldo Cruz Institute - Oswaldo Cruz Foundation (IOC-FIOCRUZ), Rio de Janeiro, Brazil.
Marcelo Felippe SantiagoLaboratory of Molecular Biology and Biochemistry of Proteins, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Robson Coutinho-SilvaLaboratory of Immunophysiology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Luiz Eduardo Baggio SavioLaboratory of Immunophysiology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Eleonora KurtenbachLaboratory of Molecular Biology and Biochemistry of Proteins, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Universidade Federal do Rio de Janeiro · BRFundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro · BRFundação Oswaldo Cruz · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The P2X7 receptor is a critical purinergic receptor in immune cells. Its activation was associated with cathepsin release into macrophage cytosol, suggesting its involvement in lysosomal membrane permeabilization (LMP) and leakage. Nevertheless, the mechanisms by which P2X7 receptor activation induces LMP and leakage are unclear. This study investigated cellular mechanisms associated with endosomal and lysosomal leakage triggered by P2X7 receptor activation. We found that ATP at 500 μM and 5 mM (but not 50 μM) induced LMP in non-stimulated peritoneal macrophages. This effect was not observed in P2X7-deficient or A740003-pretreated macrophages. We found that the P2X7 receptor and pannexin-1 channels mediate calcium influx that might be important for activating specific ion channels (TRPM2 and two-pore channels) on the membranes of late endosomes and lysosomes leading to LMP leakage and consequent cathepsin release. These findings suggest the critical role of the P2X7 receptor in inflammatory and infectious diseases

Indexed as

CalciumReceptors, Purinergic P2X7CathepsinsConnexinsLysosomesNerve Tissue ProteinsCalciumCathepsinsConnexinsNerve Tissue ProteinsReceptors, Purinergic P2X7cathepsinsextracellular ATPlysosomal permeabilizationlysosomesP2 receptor

Identifiers

PMID35222364
PMCPMC8863609
OpenAlexW4211138773

What OpenQuestion holds

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Registered trials

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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.