Evidence map›Paper›PMID 31664678›Full record

ArticleNeuroscience bulletin2020

Role of Elevated Thrombospondin-1 in Kainic Acid-Induced Status Epilepticus.

Yurong Zhang, Mengdi Zhang, Wei Zhu, Xiaohong Pan, Qiaoyun Wang, Xue Gao, Chaoyun Wang, Xiuli Zhang, Yuxia Liu, Shucui Li and 1 more

Open access · greenAbstract read
In one paragraph

Article in Neuroscience bulletin, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Yurong ZhangSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Mengdi ZhangSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Wei ZhuShandong Academy of Medical Sciences, Jinan, 250062, China.
Xiaohong PanSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Qiaoyun WangSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Xue GaoSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Chaoyun WangSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Xiuli ZhangSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Yuxia LiuSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Shucui LiSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Hongliu SunSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China. sun_china6@163.com.ORCID http://orcid.org/0000-0002-4753-5219
Binzhou Medical University · CNShandong First Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have suggested that thrombospondin-1 (TSP-1) regulates the transforming growth factor beta 1 (TGF-β1)/phosphorylated Smad2/3 (pSmad2/3) pathway. Moreover, TSP-1 is closely associated with epilepsy. However, the role of the TSP-1-regulated TGF-β1/pSmad2/3 pathway in seizures remains unclear. In this study, changes in this pathway were assessed following kainic acid (KA)-induced status epilepticus (SE) in rats. The results showed that increases in the TSP-1/TGF-β1/pSmad2/3 levels spatially and temporally matched the increases in glial fibrillary acidic protein (GFAP)/chondroitin sulfate (CS56) levels following KA administration. Inhibition of TSP-1 expression by small interfering RNA or inhibition of TGF-β1 activation with a Leu-Ser-Lys-Leu peptide significantly reduced the severity of KA-induced acute seizures. These anti-seizure effects were accompanied by decreased GFAP/CS56 expression and Smad2/3 phosphorylation. Moreover, inhibiting Smad2/3 phosphorylation with ponatinib or SIS3 also significantly reduced seizure severity, alongside reducing GFAP/CS56 immunoreactivity. These results suggest that the TSP-1-regulated TGF-β1/pSmad2/3 pathway plays a key role in KA-induced SE and astrogliosis, and that inhibiting this pathway may be a potential anti-seizure strategy.

Indexed as

Signal TransductionAnimalsChondroitin SulfatesDisease Models, AnimalExcitatory Amino Acid AgonistsGlial Fibrillary Acidic ProteinImidazolesIsoquinolinesKainic AcidMaleProtein Kinase InhibitorsPyridazinesPyridinesPyrrolesRatsRats, Sprague-Dawley6,7-dimethyl-2-(2E)-3-(1-methyl-2-phenyl-1H-pyrrolo(2,3-b)pyridin-3-yl-prop-2-enoyl)-1,2,3,4-tetrahydroisoquinoline hydrochlorideChondroitin SulfatesExcitatory Amino Acid AgonistsGfap protein, ratGlial Fibrillary Acidic ProteinImidazolesIsoquinolinesKainic AcidponatinibProtein Kinase InhibitorsPyridazinesPyridinesPyrrolesSmad2 ProteinSmad2 protein, ratSmad3 ProteinSmad3 protein, ratTgfb1 protein, ratThbs1 protein, ratThrombospondin 1Transforming Growth Factor beta1AstrogliosisPonatinibStatus epilepticusThrombospondin-1

Identifiers

PMID31664678
PMCPMC7056766
OpenAlexW2982443775

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.