Evidence map›Paper›PMID 33530496›Full record

ArticleInternational journal of molecular sciences2021

Hypoxia-Induced S100A8 Expression Activates Microglial Inflammation and Promotes Neuronal Apoptosis.

Ji Sun Ha, Hye-Rim Choi, In Sik Kim, Eun-A Kim, Sung-Woo Cho, Seung-Ju Yang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  4. Roles of the Altitude-Adapted Immune Microenvironment in Pulmonary Vascular Remodeling in High-Altitude Pulmonary Hypertension: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026
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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 3 institutions in 1 country.

Ji Sun HaDepartment of Biomedical Laboratory Science, Konyang University, Daejeon 35365, Korea.
Hye-Rim ChoiDepartment of Biomedical Laboratory Science, Konyang University, Daejeon 35365, Korea.
In Sik KimDepartment of Biomedical Laboratory Science, School of Medicine, Eulji University, Uijeongbu 11759, Korea.
Eun-A KimDepartment of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 05505, Korea.
Sung-Woo ChoDepartment of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 05505, Korea.
Seung-Ju YangDepartment of Biomedical Laboratory Science, Konyang University, Daejeon 35365, Korea.ORCID 0000-0001-9261-2749
Konyang University · KRUlsan College · KREulji University · KR

Funding

Ministry of Education 2018R1D1A3A03000692Ministry of Science and ICT, South Korea 2018R1A2B6001743
6 · The paper itself

Abstract

S100 calcium-binding protein A8 (S100A8), a danger-associated molecular pattern, has emerged as an important mediator of the pro-inflammatory response. Some S100 proteins play a prominent role in neuroinflammatory disorders and increase the secretion of pro-inflammatory cytokines in microglial cells. The aim of this study was to determine whether S100A8 induced neuronal apoptosis during cerebral hypoxia and elucidate its mechanism of action. In this study, we reported that the S100A8 protein expression was increased in mouse neuronal and microglial cells when exposed to hypoxia, and induced neuroinflammation and neuronal apoptosis. S100A8, secreted from neurons under hypoxia, activated the secretion of tumor necrosis factor (TNF-α) and interleukin-6 (IL-6) through phosphorylation of extracellular-signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) in microglia. Also, phosphorylation of ERK via the TLR4 receptor induced the priming of the NLRP3 inflammasome. The changes in Cyclooxygenase-2 (COX-2) expression, a well-known inflammatory activator, were regulated by the S100A8 expression in microglial cells. Knockdown of S100A8 levels by using shRNA revealed that microglial S100A8 expression activated COX-2 expression, leading to neuronal apoptosis under hypoxia. These results suggested that S100A8 may be an important molecule for bidirectional microglia-neuron communication and a new therapeutic target for neurological disorders caused by microglial inflammation during hypoxia.

Indexed as

Gene Expression RegulationAnimalsApoptosisBiomarkersCalgranulin ACell LineCytokinesDisease SusceptibilityExtracellular Signal-Regulated MAP KinasesGene Knockdown TechniquesHypoxiaInflammationInflammation MediatorsJNK Mitogen-Activated Protein KinasesMiceMicrogliaBiomarkersCalgranulin ACytokinesExtracellular Signal-Regulated MAP KinasesInflammation MediatorsJNK Mitogen-Activated Protein KinasesS100a8 protein, mouseCOX-2hypoxiainflammasomemicroglianeuronal apoptosisS100A8

Identifiers

PMID33530496
PMCPMC7866104
OpenAlexW3123714645

What OpenQuestion holds

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LicenceCC BY
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.