Evidence map›Paper›PMID 29844306›Full record

ArticleCell death & disease2018

S100A11 protects against neuronal cell apoptosis induced by cerebral ischemia via inhibiting the nuclear translocation of annexin A1.

Qian Xia, Xing Li, Huijuan Zhou, Lu Zheng, Jing Shi

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

47 citing papers in PubMed, 105 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Annexin A1: The dawn of ischemic stroke (Review).Molecular medicine reports · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. CAM-A-dependent HBV core aggregation induces apoptosis through ANXA1.JHEP reports : innovation in hepatology · 2024
    Article
  9. Article
  10. Article
  11. The Sirtuin 5 Inhibitor MC3482 Ameliorates Microglia‑induced Neuroinflammation Following Ischaemic Stroke by Upregulating the Succinylation Level of Annexin-A1.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
    Article
  12. Article
  13. Article
  14. Annexin A1 in the nervous and ocular systems.Neural regeneration research · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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.

Qian XiaDepartment of Neurobiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Xing LiDepartment of Neurobiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Huijuan ZhouDepartment of Neurobiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Lu ZhengDepartment of Neurobiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Jing ShiDepartment of Neurobiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China. sj@mails.tjmu.edu.cn.
Huazhong University of Science and Technology · CNMinistry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The subcellular location of annexin A1 (ANXA1) determines the ultimate fate of neurons after ischemic stroke. ANXA1 nuclear translocation is involved in neuronal apoptosis after cerebral ischemia, and extracellular ANXA1 is also associated with regulation of inflammatory responses. As the factors and mechanism that influence ANXA1 subcellular translocation remain unclear, studies aiming to determine and clarify the role of ANXA1 as a cell fate 'regulator' within cells are critically needed. In this study, we found that intracerebroventricular injection of the recombinant adenovirus vector Ad-S100A11 (carrying S100A11) strongly improved cognitive function and induced robust neuroprotective effects after ischemic stroke in vivo. Furthermore, upregulation of S100A11 protected against neuronal apoptosis induced by oxygen-glucose deprivation and reoxygenation (OGD/R) in vitro. Surprisingly, S100A11 overexpression markedly decreased ANXA1 nuclear translocation and subsequently alleviated OGD/R-induced neuronal apoptosis. Notably, S100A11 exerted its neuroprotective effect by directly binding ANXA1. Importantly, S100A11 directly interacted with ANXA1 through the nuclear translocation signal (NTS) of ANXA1, which is essential for ANXA1 to import into the nucleus. Consistent with our previous studies, ANXA1 nuclear translocation after OGD/R promoted p53 transcriptional activity, induced mRNA expression of the pro-apoptotic Bid gene, and activated the caspase-3 apoptotic pathway, which was almost completely reversed by S100A11 overexpression. Thus, S100A11 protects against cell apoptosis by inhibiting OGD/R-induced ANXA1 nuclear translocation. This study provides a novel mechanism whereby S100A11 protects against neuronal cells apoptosis, suggesting the potential for a previously unidentified treatment strategy in minimizing apoptosis after ischemic stroke.

Indexed as

ApoptosisAnimalsAnnexin A1Behavior, AnimalBrain IschemiaCell MembraneCell NucleusCell SurvivalGlucoseMaleMembrane ProteinsMemoryMiceMice, Inbred C57BLModels, BiologicalMotor ActivityAnnexin A1GlucoseMembrane ProteinsNeuroprotective AgentsOxygenPex14 protein, mouseRepressor ProteinsS100A11 protein, mouseS100 Proteins

Identifiers

PMID29844306
PMCPMC5974363
OpenAlexW2807660866

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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.