Evidence map›Paper›PMID 30221695›Full record

ArticleMolecular medicine reports2018

CXCL12 induces migration of oligodendrocyte precursor cells through the CXCR4‑activated MEK/ERK and PI3K/AKT pathways.

Yongyang Tian, Hong Yin, Xi Deng, Beichuan Tang, Xianjun Ren, Tao Jiang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.3field-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

31 citing papers in PubMed, 48 citations in OpenAlex.

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  9. Spatiotemporal transcriptomic map of glial cell response in a mouse model of acute brain ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

6 authors at 1 institution in 1 country.

Yongyang TianDepartment of Orthopedics, Third Military Medical University (Army Medical University), Chongqing 400037, P.R. China.
Hong YinDepartment of Orthopedics, Third Military Medical University (Army Medical University), Chongqing 400037, P.R. China.
Xi DengDepartment of Ultrasound, Xinqiao Hospital, Third Military Medical University (Army Medical University), Chongqing 400037, P.R. China.
Beichuan TangDepartment of Orthopedics, Third Military Medical University (Army Medical University), Chongqing 400037, P.R. China.
Xianjun RenDepartment of Orthopedics, Third Military Medical University (Army Medical University), Chongqing 400037, P.R. China.
Tao JiangDepartment of Orthopedics, Third Military Medical University (Army Medical University), Chongqing 400037, P.R. China.
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Demyelination is a nervous system disease in which the myelin sheaths of neurons are damaged due to inflammatory reactions, inherited abnormalities or trauma. This damage impairs the conduction of signals in the affected nerves, which in turn causes deficiencies in sensation, movement and cognition. Oligodendrocyte precursor cells (OPCs) are able to induce remyelination. However, the remyelination is suboptimal due to the limited migration of OPCs. In the present study, neonatal OPCs were isolated from rats for the investigation of the role of C‑X‑C motif chemokine ligand 12 (CXCL12), an important chemokine, in mediating the migration ability of OPCs. The present results demonstrated that CXCL12 stimulation markedly promoted the migration of OPCs and activated the dual specificity mitogen‑activated protein kinase kinase 1 (MEK)/extracellular signal‑regulated kinase (ERK) and phosphoinositide 3‑kinase (PI3K)/RAC‑α serine/threonine‑protein kinase (AKT) pathways. Knockdown of C‑X‑C motif chemokine receptor 4 (CXCR4; a receptor of CXCL12) reversed the CXCL12‑induced migration of OPCs and blocked the MEK/ERK and PI3K/AKT pathways. In addition, specific inhibitors of the MEK/ERK and PI3K/AKT pathways significantly reduced the migration of OPCs. Based on these findings, it was concluded that CXCL12 may induce the migration of OPCs through the CXCR4‑activated MEK/ERK and PI3K/AKT pathways. The results of the present study support the manipulation of CXCL12‑mediated OPC migration to improve remyelination.

Indexed as

AnimalsCell MovementChemokine CXCL12Demyelinating DiseasesHumansInflammationMAP Kinase Kinase 1Myelin SheathNervous System DiseasesOligodendrocyte Precursor CellsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsReceptors, CXCR4RemyelinationChemokine CXCL12CXCL12 protein, ratCxcr4 protein, ratMAP Kinase Kinase 1Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, CXCR4

Identifiers

PMID30221695
PMCPMC6172403
OpenAlexW2889196675

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.