Evidence map›Paper›PMID 23416151›Full record

ArticleBrain research2013

Microglial CD14 activated by iNOS contributes to neuroinflammation in cerebral ischemia.

Mian Zhou, Christie M Wang, Weng-Lang Yang, Ping Wang

Abstract read
In one paragraph

Article in Brain research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.5field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Pharmaceuticals (Basel, Switzerland) · 2026
    Article
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  14. Article
  15. Dysregulation of IGF-1/GLP-1 signaling in the progression of ALS: potential target activators and influences on neurological dysfunctions.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Neuroinflammation: friend and foe for ischemic stroke.Journal of neuroinflammation · 2019
    Review
  20. 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.

Mian ZhouDepartment of Surgery, Hofstra North Shore-LIJ School of Medicine, The Feinstein Institute for Medical Research, Manhasset, NY 11030, USA.
Christie M Wang
Weng-Lang Yang
Ping Wang
Feinstein Institute for Medical Research · US

Funding

IMPROVEMENT OF ORGAN FUNCTION AFTER SEVERE HYPOVOLEMIAR01HL076179 · NHLBI · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI PING WANG · 2004 to 2026
$7.6M
SEPSIS--MEDIATORS AND CARDIOVASCULAR RESPONSESR01GM057468 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WANG, PING · 1998 to 2015
$3.8M
Modulation of Hepatocellular Function in SepsisR01GM053008 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WANG, PING · 2001 to 2015
$3.7M
NHLBI NIH HHS R01 HL076179NHLBI NIH HHS R01HL076179NIGMS NIH HHS R01 GM053008NIGMS NIH HHS R01GM053008NIGMS NIH HHS R01 GM057468NIGMS NIH HHS R01GM057468
6 · The paper itself

Abstract

Stroke is one of the most frequent causes of death and disability worldwide. Cerebral ischemia is the major insult of stroke and induces acute inflammation by triggering excessive production of proinflammatory cytokines, leading to the exacerbation of primary brain damage. Toll-like receptor (TLR)- and nitric oxide-mediated signaling pathways have been identified under ischemic stress. However, the interaction between these two pathways in controlling proinflammatory cytokines has not been well addressed during cerebral ischemia. Adult male C57BL/6 mice were subjected to middle cerebral artery occlusion (MCAO) for stroke induction. The MCAO procedure resulted in a significant infarct in the brain after 24h. The infarcted side of the brain had marked elevation of TNF-α gene and protein expression, compared to the sham brain. The expression of CD14, a co-receptor of TLR4, was induced by MCAO, while the expression of TLR4 remained unchanged. The levels of inducible nitric oxide synthase (iNOS) and nitrotyrosine were also upregulated in the infracted side of the brain. Correspondingly, exposing murine microglial BV2 cells to hypoxia (1% O2) for 20h resulted in an increased expression of TNF-α, CD14, iNOS, and nitrotyrosine. When BV2 cells were treated with l-canavanine, an iNOS selective inhibitor, the elevation of TNF-α and CD14 induced by hypoxia was inhibited. This inhibition was associated with an increase of IκB. These results suggest that the upregulation of TNF-α production in ischemic stroke is partially through increasing iNOS, and then CD14 expression leading to the activation of the NF-κB pathway in microglia.

Indexed as

AnimalsBlotting, WesternBrain IschemiaDisease Models, AnimalInflammationLipopolysaccharide ReceptorsMaleMiceMice, Inbred C57BLMicrogliaNF-kappa BNitric Oxide Synthase Type IIReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionSignal TransductionTumor Necrosis Factor-alphaLipopolysaccharide ReceptorsNF-kappa BNitric Oxide Synthase Type IINos2 protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID23416151
PMCPMC3615048
OpenAlexW2001073644

What OpenQuestion holds

Textmetadata
LicenceTDM
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.