Evidence map›Paper›PMID 28586011›Full record

ArticleMolecular medicine reports2017

Microglia activation triggers oligodendrocyte precursor cells apoptosis via HSP60.

Yunhong Li, Rui Zhang, Xiaolin Hou, Yumei Zhang, Feijia Ding, Fan Li, Yao Yao, Yin Wang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
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  14. Regulation of microglia function by neural stem cells.Frontiers in cellular neuroscience · 2023
    Review
  15. NG2-glia crosstalk with microglia in health and disease.CNS neuroscience & therapeutics · 2022
    Review
  16. Article
  17. Review
  18. Review
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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 1 institution in 1 country.

Yunhong LiNingxia Key Laboratory of Cerebrocranial Diseases, Basic Medical College of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Rui ZhangNingxia Key Laboratory of Cerebrocranial Diseases, Basic Medical College of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Xiaolin HouDepartment of Neurology, The General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Yumei ZhangNingxia Key Laboratory of Cerebrocranial Diseases, Basic Medical College of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Feijia DingNingxia Key Laboratory of Cerebrocranial Diseases, Basic Medical College of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Fan LiNingxia Key Laboratory of Cerebrocranial Diseases, Basic Medical College of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Yao YaoNingxia Key Laboratory of Cerebrocranial Diseases, Basic Medical College of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Yin WangNingxia Key Laboratory of Cerebrocranial Diseases, Basic Medical College of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Ningxia Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive microglia are present in lesions of myelin‑associated white matter disorders resulting in injuries to oligodendrocyte precursor cells (OPCs). Therefore, protection of OPCs from injury due to excessive activation of microglia is important in treating these diseases. Heat shock protein 60 (HSP60) has been demonstrated to be released extracellularly in the failing heart upon stress or injury. However, the role of HSP60 in the central nervous system and whether it participates in the toxic effects of microglia on OPCs remains unclear. The present study used the co‑culture, cell death assays, binding assays, immunochemistry, western blot and ELISA. HSP60 was demonstrated to be released extracellularly by LPS‑activated microglia and to bind to OPCs, triggering OPC apoptosis. When pretreated with toll‑like receptor (TLR) 4 blocking antibody, the viability of OPCs increased, while the expression of nuclear factor κB (NFκB), caspase 3 and the release of proinflammatory cytokines triggered by HSP60 decreased. These results suggest that HSP60 released by microglia may mediate OPC apoptosis through binding to TLR4 on the surface of OPCs and subsequently activating the TLR4‑NFκB signaling pathway. HSP60 may, therefore, serve as a potential target for treatment of myelin‑associated neurodegenerative diseases that are accompanied by microglia activation.

Indexed as

ApoptosisAnimalsCaspase 3Cells, CulturedChaperonin 60Coculture TechniquesCytokinesGene ExpressionMaleMicrogliaOligodendrocyte Precursor CellsProtein BindingRatsToll-Like Receptor 4Caspase 3Chaperonin 60CytokinesToll-Like Receptor 4

Identifiers

PMID28586011
PMCPMC5482110
OpenAlexW2619420073

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.