Evidence map›Paper›PMID 25966946›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2015

CX3CL1/CX3CR1-mediated microglia activation plays a detrimental role in ischemic mice brain via p38MAPK/PKC pathway.

Yong Liu, Xiao-Mei Wu, Qian-Qian Luo, Suna Huang, Qing-Wu Qian Yang, Fa-Xiang Wang, Ya Ke, Zhong-Ming Qian

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing 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

52 citing papers in PubMed, 84 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

8 authors at 4 institutions in 1 country.

Yong LiuDepartment of Neurology, Xinqiao Hospital, The Third Military Medical University, Chongqing, China.
Xiao-Mei WuDepartment of Neurobiology, Institute for Nautical Medicine, Nantong University, Nantong, China.
Qian-Qian LuoDepartment of Neurobiology, Institute for Nautical Medicine, Nantong University, Nantong, China.
Suna HuangLaboratory of Neuropharmacology, Fudan University School of Pharmacy, Pu Dong, Shanghai, China.
Qing-Wu Qian YangDepartment of Neurology, Xinqiao Hospital, The Third Military Medical University, Chongqing, China.
Fa-Xiang WangDepartment of Neurology, Xinqiao Hospital, The Third Military Medical University, Chongqing, China.
Ya KeSchool of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, New Territories, Hong Kong, China.
Zhong-Ming QianDepartment of Neurobiology, Institute for Nautical Medicine, Nantong University, Nantong, China.
Army Medical University · CNFudan University · CNNantong University · CNChinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The exact roles of activated microglia and fractalkine (CX3CL1)/fractalkine receptor (CX3CR1) signaling are not fully understood in brain ischemic injury and the findings reported are controversial. Here, we investigated the effects of CX3CR1 siRNA on the expression of CX3CR1, p38 mitogen-activated protein kinase (p38MAPK), Protein Kinase C (PKC) and inflammatory cytokines, microglia activation, white matter lesions, and cognitive function in mice treated with bilateral common carotid artery stenosis (BCAS) in vivo as well as effects of exogenous CX3CL1, CX3CR1 siRNA, and SB2035080 on expression of inflammatory cytokines in BV2 microglia treated with oxygen-glucose deprivation (OGD) in vitro. We showed that CX3CR1 siRNA significantly inhibited the increased expression of CX3CR1, p38MAPK, PKC as well as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6, and also attenuated microglia activation, white matter lesions, and cognitive deficits induced by BCAS in mice brain. We also showed that exogenous CX3CL1 could induce a further enhancement in TNF-α and IL-1β expression, which could be suppressed by CX3CR1 siRNA or by the p38MAPK inhibitor in OGD-treated BV2 microglial cells in vitro. Our findings indicated that CX3CL1/CX3CR1-mediated microglial activation plays a detrimental role in ischemic brain via p38MAPK/PKC signaling and also suggested that CX3CL1/CX3CR1 axis might be a putative therapeutic target to disrupt the cascade of deleterious events that lead to brain ischemic injury.

Indexed as

Chemokine CX3CL1Macrophage ActivationMicrogliap38 Mitogen-Activated Protein KinasesProtein Kinase CReceptors, ChemokineSignal TransductionAnimalsBrainBrain IschemiaCarotid StenosisCX3C Chemokine Receptor 1GlucoseHypoxia, BrainInjections, IntraventricularInterleukin-1betaChemokine CX3CL1CX3C Chemokine Receptor 1Cx3cl1 protein, mouseCx3cr1 protein, mouseGlucoseInterleukin-1betap38 Mitogen-Activated Protein KinasesProtein Kinase CReceptors, ChemokineTumor Necrosis Factor-alpha

Identifiers

PMID25966946
PMCPMC4640309
OpenAlexW1435754940

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.