Evidence map›Paper›PMID 27873133›Full record

ArticleNeurochemical research2017

Altered Expression of CXCL13 and CXCR5 in Intractable Temporal Lobe Epilepsy Patients and Pilocarpine-Induced Epileptic Rats.

Ruohan Li, Limin Ma, Hao Huang, Shu Ou, Jinxian Yuan, Tao Xu, Xinyuan Yu, Xi Liu, Juan Yang, Yangmei Chen and 1 more

Abstract read
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Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-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

17 citing papers in PubMed, 32 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

11 authors at 1 institution in 1 country.

Ruohan LiDepartment of Neurology, Seond Affiliated Hospital of Chongqing Medical University, 74 Lin Jiang Road, Chongqing, 400010, China.
Limin MaDepartment of Neurology, Seond Affiliated Hospital of Chongqing Medical University, 74 Lin Jiang Road, Chongqing, 400010, China.
Hao HuangDepartment of Neurology, Seond Affiliated Hospital of Chongqing Medical University, 74 Lin Jiang Road, Chongqing, 400010, China.
Shu OuDepartment of Neurology, Seond Affiliated Hospital of Chongqing Medical University, 74 Lin Jiang Road, Chongqing, 400010, China.
Jinxian YuanDepartment of Neurology, Seond Affiliated Hospital of Chongqing Medical University, 74 Lin Jiang Road, Chongqing, 400010, China.
Tao XuDepartment of Neurology, Seond Affiliated Hospital of Chongqing Medical University, 74 Lin Jiang Road, Chongqing, 400010, China.
Xinyuan YuDepartment of Neurology, Seond Affiliated Hospital of Chongqing Medical University, 74 Lin Jiang Road, Chongqing, 400010, China.
Xi LiuDepartment of Neurology, Seond Affiliated Hospital of Chongqing Medical University, 74 Lin Jiang Road, Chongqing, 400010, China.
Juan YangDepartment of Neurology, Seond Affiliated Hospital of Chongqing Medical University, 74 Lin Jiang Road, Chongqing, 400010, China.
Yangmei ChenDepartment of Neurology, Seond Affiliated Hospital of Chongqing Medical University, 74 Lin Jiang Road, Chongqing, 400010, China.
Xi PengDepartment of Neurology, Seond Affiliated Hospital of Chongqing Medical University, 74 Lin Jiang Road, Chongqing, 400010, China. px5523@126.com.
Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms that underlie the pathogenesis of epilepsy are still unclear. Recent studies have indicated that inflammatory processes occurring in the brain are involved in a common and crucial mechanism in epileptogenesis. C-X-C motif chemokine ligand 13 (CXCL13) and its only receptor, C-X-C motif chemokine receptor 5 (CXCR5), are highly expressed in the central nervous system (CNS) and participate in inflammatory responses. The present study aimed to assess the expression of CXCL13 and CXCR5 in the brain tissues of both patients with intractable epilepsy (IE) and a rat model (lithium-pilocarpine) of temporal lobe epilepsy (TLE) to identify possible roles of the CXCL13-CXCR5 signaling pathway in epileptogenesis. Real-time quantitative polymerase chain reaction (RT-qPCR), immunohistochemical, double-labeled immunofluorescence and Western blot analyses were performed in this study. CXCL13 and CXCR5 mRNA expression and protein levels were found to be significantly up-regulated in the TLE patients and TLE rats. Further, CXCL13 and CXCR5 protein levels were altered during the different epileptic phases after onset of status epilepticus (SE) in the pilocarpine model rats, including the acute phase (6, 24, and 72 h), latent phase (7 and 14 days) and chronic phase (30 and 60 days groups). Moreover, double-labeled immunofluorescence analysis revealed that CXCL13 was mainly expressed in the cytomembranes and cytoplasm of neurons and astrocytes, while CXCR5 was mainly expressed in the cytomembranes and cytoplasm of neurons. Thus, the CXCL13-CXCR5 signaling pathway may play a possible pathogenic role in IE. CXCL13 and CXCR5 may represent potential biomarkers of brain inflammation in epileptic patients.

Indexed as

AdolescentAdultAnimalsBiomarkersChemokine CXCL13ChildEpilepsyEpilepsy, Temporal LobeFemaleGene Expression RegulationHumansMaleMiddle AgedNeocortexPilocarpineRatsBiomarkersChemokine CXCL13CXCL13 protein, humanCXCR5 protein, humanPilocarpineReceptors, CXCR5ChemokinesCXCL13CXCR5InflammationPilocarpineTemporal lobe epilepsy

Identifiers

PMID27873133
OpenAlexW2550414352

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Registered trials

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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.