Evidence map›Paper›PMID 32819386›Full record

ArticleJournal of neuroinflammation2020

Myeloid Pannexin-1 mediates acute leukocyte infiltration and leads to worse outcomes after brain trauma.

Joon Ho Seo, Miloni S Dalal, Frances Calderon, Jorge E Contreras

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  8. Astrocyte and neuronal Panx1 support long-term reference memory in mice.bioRxiv : the preprint server for biology · 2023
    Article
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  13. Pannexin-1 Channels as Mediators of Neuroinflammation.International journal of molecular sciences · 2021
    Review
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  15. 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 1 institution in 1 country.

Joon Ho SeoDepartment of Pharmacology, Physiology and Neuroscience, New Jersey Medical School, Rutgers University, Medical Sciences Building I-615; 185 S. Orange Avenue, Newark, NJ, 07103, USA.
Miloni S DalalDepartment of Pharmacology, Physiology and Neuroscience, New Jersey Medical School, Rutgers University, Medical Sciences Building I-615; 185 S. Orange Avenue, Newark, NJ, 07103, USA.
Frances CalderonDepartment of Pharmacology, Physiology and Neuroscience, New Jersey Medical School, Rutgers University, Medical Sciences Building I-615; 185 S. Orange Avenue, Newark, NJ, 07103, USA.
Jorge E ContrerasDepartment of Pharmacology, Physiology and Neuroscience, New Jersey Medical School, Rutgers University, Medical Sciences Building I-615; 185 S. Orange Avenue, Newark, NJ, 07103, USA. contrejo@njms.rutgers.edu.ORCID http://orcid.org/0000-0001-7690-4231
Rutgers, The State University of New Jersey · US

Funding

New Jersey Commission on Brain Injury Research CBIR19IRG014
6 · The paper itself

Abstract

backgroundNeuroinflammation is a major component of secondary damage after traumatic brain injury (TBI). We recently reported that pharmacological inhibition of Pannexin-1 (Panx1) channels markedly reduced the inflammatory response after TBI. Panx1 channels have been shown to be important conduits for adenosine 5'-triphosphate (ATP) release and are associated with leukocyte infiltration and pyroptosis. Because Panx1 blockers significantly decrease ATP release and migration of activated microglia and other myeloid cells (such as monocyte-derived macrophages and dendritic cells) in vitro, we hypothesized that myeloid Panx1 channels play a specific role in immune cell infiltration promoting tissue damage following TBI.

methodsThe murine-controlled cortical impact (CCI) model was used on myeloid-specific Panx1 conditional knockout (Cx3cr1-Cre::Panx1

resultsCCI-injured Cx3cr1-Cre::Panx1

conclusionOur data demonstrate that CCI-related outcomes correlate with Panx1 channel function in myeloid cells, indicating that activation of Panx1 channels in myeloid cells is a major contributor to acute brain inflammation following TBI. Importantly, our data indicate myeloid Panx1 channels could serve as an effective therapeutic target to improve outcome after TBI.

Indexed as

AnimalsBrainBrain Injuries, TraumaticConnexinsDisease Models, AnimalLeukocytesLocomotionMaze LearningMiceMice, KnockoutMyeloid CellsNerve Tissue ProteinsPrognosisRotarod Performance TestConnexinsNerve Tissue ProteinsPanx1 protein, mouseBlood–brain barrierHemichannelsInflammationPannexinTraumatic brain injury

Identifiers

PMID32819386
PMCPMC7441665
OpenAlexW3057914820

What OpenQuestion 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 OpenQuestion graph.