Evidence map›Paper›PMID 34792689›Full record

ArticleCell biology and toxicology2023

Autocrine S100B in astrocytes promotes VEGF-dependent inflammation and oxidative stress and causes impaired neuroprotection.

Saidan Ding, Chengde Wang, Weikan Wang, He Yu, Baihui Chen, Leping Liu, Minxue Zhang, Yan Lang

Abstract read
PubMed Publisher
In one paragraph

Article in Cell biology and toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

19 citing papers in PubMed, 22 citations in OpenAlex.

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  9. Reactive Astrocytes in Glioma: Emerging Opportunities and Challenges.International journal of molecular sciences · 2025
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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 3 institutions in 2 countries.

Saidan Ding *Central Laboratory, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. firstdsdan@hotmail.com.
Chengde Wang *Neurosurgery department, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Weikan Wang *Department of Microbiology, Immunology and Genetics, University of North Texas Health Science Center, Fort Worth, TX, 76107, USA.
He Yu *Central Laboratory, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Baihui Chen *Central Laboratory, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Leping Liu *Central Laboratory, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Minxue ZhangCentral Laboratory, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Yan LangCentral Laboratory, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
First Affiliated Hospital of Wenzhou Medical University · CNUniversity of North Texas Health Science Center · USWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Minimal hepatic encephalopathy (MHE) is strongly associated with neuroinflammation. Nevertheless, the underlying mechanism of the induction of inflammatory response in MHE astrocytes remains not fully understood. In the present study, we investigated the effect and mechanism of S100B, a predominant isoform expressed and released from mature astrocytes, on MHE-like neuropathology in the MHE rat model. We discovered that S100B expressions and autocrine were significantly increased in MHE rat brains and MHE rat brain-derived astrocytes. Furthermore, S100B stimulates VEGF expression via the interaction between TLR2 and RAGE in an autocrine manner. S100B-facilitated VEGF autocrine expression further led to a VEGFR2 and COX-2 interaction, which in turn induced the activation of NFƙB, eventually resulting in inflammation and oxidative stress in MHE astrocytes. MHE astrocytes supported impairment of neuronal survival and growth in a co-culture system. To sum up, a comprehensive understanding of the role of S100B-overexpressed MHE astrocyte in MHE pathogenesis may provide insights into the etiology of MHE.

Indexed as

AstrocytesAnimalsInflammationNeuroprotectionOxidative StressRatsS100 Calcium Binding Protein beta SubunitVascular Endothelial Growth FactorsS100b protein, ratS100 Calcium Binding Protein beta SubunitVascular Endothelial Growth FactorsAstrocytesCognitive impairmentInflammationS100 calcium-binding protein B (S100B)Vascular endothelial growth factor (VEGF)

Identifiers

PMID34792689
OpenAlexW3136465485

What OpenQuestion holds

Textmetadata
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.