Evidence map›Paper›PMID 28912678›Full record

ArticleFrontiers in molecular neuroscience2017

IL-17A Enhances Microglial Response to OGD by Regulating p53 and PI3K/Akt Pathways with Involvement of ROS/HMGB1.

Bin Zhang, Ning Yang, Zhi-Ming Mo, Shao-Peng Lin, Feng Zhang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Observational
  5. Review
  6. Article
  7. Th17 Cells and IL-17A in Ischemic Stroke.Molecular neurobiology · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  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

5 authors at 2 institutions in 1 country.

Bin ZhangDepartment of Neurology, the Fifth Affiliated Hospital of Guangzhou Medical UniversityGuangzhou, China.
Ning YangDepartment of Neurology, the Fifth Affiliated Hospital of Guangzhou Medical UniversityGuangzhou, China.
Zhi-Ming MoDepartment of Neurology, the Fifth Affiliated Hospital of Guangzhou Medical UniversityGuangzhou, China.
Shao-Peng LinDepartment of Emergency, the Second Affiliated Hospital of Guangzhou Medical UniversityGuangzhou, China.
Feng ZhangDepartment of Neurosurgery, the Fourth Affiliated Hospital of Guangzhou Medical UniversityGuangzhou, China.
Guangzhou Medical University · CNSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral ischemia-reperfusion injury (IRI) has a complex pathogenesis, and interleukin-17 (IL-17) is a newly identified class of the cytokine family that plays an important role in ischemic inflammation. An oxygen-glucose deprivation (OGD) model showed that IL-17A expression was significantly up-regulated in microglial cells. After IL-17A siRNA transfection, the inhibition of proliferation, and the increased apoptosis in microglial cells, induced by OGD/reperfusion, was improved, and the elevation of Caspase-3, Caspase-8, Caspase-9, and poly ADP ribose polymerase (PARP) activities was inhibited. Mass spectrometry demonstrated that IL-17A functioned through a series of factors associated with oxidative stress and apoptosis and regulated Caspase-3 activity and apoptosis in microglial cells via the p53 and PI3K/Akt signaling pathways. IL-17A, HMGB1, and ROS were regulated mutually to exhibit a synergistic effect in the OGD model of microglial cells, but the down-regulation of IL-17A or HMGB1 expression did not completely inhibit the production of ROS. These findings demonstrated that ROS might be located upstream of IL-17A and HMGB1 so that ROS can regulate HMGB1/IL-17A expression to affect the p53 and PI3K/Akt signaling pathways and therefore promote the occurrence of apoptosis in microglial cells. These findings provide a novel evidence for the role of IL-17A in ischemic cerebral diseases.

Indexed as

cerebral ischemia-reperfusion injuryHMGB1IL-17Amass spectrometrymicroglial cellsproteomicsreactive oxygen species

Identifiers

PMID28912678
PMCPMC5583146
OpenAlexW2752244624

What OpenQuestion holds

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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.