Evidence map›Paper›PMID 25972240›Full record

ArticleMolecular neurobiology2016

Activation and Regulation of NLRP3 Inflammasome by Intrathecal Application of SDF-1a in a Spinal Cord Injury Model.

Adib Zendedel, Sonja Johann, Soraya Mehrabi, Mohammad-Taghi Joghataei, Gholamreza Hassanzadeh, Markus Kipp, Cordian Beyer

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

92 citing papers in PubMed, 185 citations in OpenAlex.

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  18. Neuroadaptive Biochemical Mechanisms of Remote Ischemic Conditioning.International journal of molecular sciences · 2023
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32 more citing papers are in PubMed but not listed here.

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 5 institutions in 2 countries.

Adib ZendedelInstitute of Neuroanatomy, RWTH Aachen University, 52074, Aachen, Germany. azendedel@ukaachen.de.
Sonja JohannInstitute of Neuroanatomy, RWTH Aachen University, 52074, Aachen, Germany.
Soraya MehrabiSchool of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Mohammad-Taghi JoghataeiDepartment of Anatomy and Neuroscience, Cellular and Molecular Research Center, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Gholamreza HassanzadehDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Markus KippInstitute of Neuroanatomy, RWTH Aachen University, 52074, Aachen, Germany.
Cordian BeyerInstitute of Neuroanatomy, RWTH Aachen University, 52074, Aachen, Germany.
RWTH Aachen University · DETehran University of Medical Sciences · IRGuilan University of Medical Sciences · IRIran University of Medical Sciences · IRLudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stromal cell-derived factor-1 alpha (SDF-1a) or CXCL12 is an important cytokine with multiple functions in the brain during development and in adulthood. The inflammatory response initiated by spinal cord injury (SCI) involves the processing of interleukin-1beta (IL-1ß) and IL-18 mediated by caspase-1 which is under the control of an intracellular multiprotein complex termed inflammasome. Using an SCI rat model, we found improved functional long-term recovery which is paralleled by a reduction of apoptosis after intrathecal treatment with SDF-1a. An intriguing aspect is that SDF-1a changed the number of neuroinflammatory cells in the damaged area. We further examined the cellular localization and sequential expression of several inflammasomes during SCI at 6 h, 24 h, 3 days, and 7 days as well as the role of SDF-1a as a regulatory factor for inflammasomes. Using 14-week old male Wistar rats, spinal cord contusion was applied at the thoracic segment 9, and animals were subsequently treated with SDF-1a via intrathecal application through an osmotic pump. SCI temporally increased the expression of the inflammasomes NLRP3, ASC, the inflammatory marker tumor necrosis factor-a (TNF-a), interleukin-1ß (IL-1β) and IL-18. SDF-1a significantly reduced the levels of IL-18, IL-1b, TNF-a, NLRP3, ASC, and caspase-1. Immunofluorescence double-labeling demonstrated that microglia and neurons are major sources of the ASC and NLRP3 respectivley. Our data provide clear evidence that SCI stimulates a complex scenario of inflammasome activation at the injured site and that SDF-1a-mediated neuroprotection presumably depends on the attenuation of the inflammasome complex.

Indexed as

AnimalsCARD Signaling Adaptor ProteinsCell CountChemokine CXCL12Disease Models, AnimalGlial Fibrillary Acidic ProteinGliosisInflammasomesInjections, SpinalLocomotionMaleMicrogliaNeuronsNLR Family, Pyrin Domain-Containing 3 ProteinRats, WistarRNA, MessengerCARD Signaling Adaptor ProteinsChemokine CXCL12Glial Fibrillary Acidic ProteinInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinPycard protein, ratRNA, MessengerAstrogliaInflammasomeMicrogliaSDF-1a (CXCL12)Spinal cord injury

Identifiers

PMID25972240
OpenAlexW2108757438

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.