Evidence map›Paper›PMID 36591943›Full record

ArticleASN neuro

Neuroprotection by Preconditioning in Mice is Dependent on MyD88-Mediated CXCL10 Expression in Endothelial Cells.

Zhihong Chen, Weiwei Hu, Mynor J Mendez, Zachary C Gossman, Anthony Chomyk, Brendan T Boylan, Grahame J Kidd, Timothy W Phares, Cornelia C Bergmann, Bruce D Trapp

Open access · goldAbstract read
In one paragraph

Article in ASN neuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Virulence · 2026
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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

10 authors at 1 institution in 2 countries.

Zhihong ChenDepartment of Neurosciences, Lerner Research Institute, 2569Cleveland Clinic, Cleveland, OH, USA.
Weiwei HuDepartment of Neurosciences, Lerner Research Institute, 2569Cleveland Clinic, Cleveland, OH, USA.
Mynor J MendezDepartment of Neurosciences, Lerner Research Institute, 2569Cleveland Clinic, Cleveland, OH, USA.ORCID 0000-0001-7899-0751
Zachary C GossmanDepartment of Neurosciences, Lerner Research Institute, 2569Cleveland Clinic, Cleveland, OH, USA.
Anthony ChomykDepartment of Neurosciences, Lerner Research Institute, 2569Cleveland Clinic, Cleveland, OH, USA.
Brendan T BoylanDepartment of Neurosciences, Lerner Research Institute, 2569Cleveland Clinic, Cleveland, OH, USA.
Grahame J KiddDepartment of Neurosciences, Lerner Research Institute, 2569Cleveland Clinic, Cleveland, OH, USA.
Timothy W PharesDepartment of Neurosciences, Lerner Research Institute, 2569Cleveland Clinic, Cleveland, OH, USA.
Cornelia C BergmannDepartment of Neurosciences, Lerner Research Institute, 2569Cleveland Clinic, Cleveland, OH, USA.
Bruce D TrappDepartment of Neurosciences, Lerner Research Institute, 2569Cleveland Clinic, Cleveland, OH, USA.ORCID 0000-0001-6682-3737
Cleveland Clinic Lerner College of Medicine · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007250 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI HUANG, ALEX YEE-CHEN · 1985 to 2023
$33.4M
Pathogenesis of Neurological Disability in Primary Diseases of MyelinR35NS097303 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI TRAPP, BRUCE D · 2017 to 2024
$6.9M
Medical Scientist Training Program at Case Western Reserve UniversityT32GM152319 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI Heather Broihier, Alex Yee-Chen Huang · 2024 to 2026
$5.1M
Regulation of B cells in the CNSR01NS086299 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI BERGMANN, CORNELIA · 2013 to 2024
$3.6M
T cell-dependent regulation of microglia demyelinating functionsR01NS110700 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI BERGMANN, CORNELIA · 2019 to 2023
$1.8M
NIGMS NIH HHS T32 GM007250NIGMS NIH HHS T32 GM152319NINDS NIH HHS R01 NS086299NINDS NIH HHS R01 NS110700NINDS NIH HHS R35 NS097303
6 · The paper itself

Abstract

The central nervous system (CNS) can be preconditioned to resist damage by peripheral pretreatment with low-dose gram-negative bacterial endotoxin lipopolysaccharide (LPS). Underlying mechanisms associated with transient protection of the cerebral cortex against traumatic brain injury include increased neuronal production of antiapoptotic and neurotrophic molecules, microglial-mediated displacement of inhibitory presynaptic terminals innervating the soma of cortical projection neurons, and synchronized firing of cortical projection neurons. However, the cell types and signaling responsible for these neuronal and microglial changes are unknown. A fundamental question is whether LPS penetrates the CNS or acts on the luminal surface of brain endothelial cells, thereby triggering an indirect parenchymal neuroprotective response. The present study shows that a low-dose intraperitoneal LPS treatment increases brain endothelial cell activation markers CD54, but does not open the blood-brain barrier or alter brain endothelial cell tight junctions as assessed by electron microscopy. NanoString nCounter transcript analyses of CD31-positive brain endothelial cells further revealed significant upregulation of

Indexed as

LipopolysaccharidesMyeloid Differentiation Factor 88AnimalsEndothelial CellsMiceMice, Inbred C57BLMice, KnockoutMicrogliaNeuroprotectionLipopolysaccharidesMyd88 protein, mouseMyeloid Differentiation Factor 88brain endothelialCXCL10LPSmicrogliaMyD88neuroprotectionTLR4

Identifiers

PMID36591943
PMCPMC9810995
OpenAlexW4313453210

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.