Evidence map›Paper›PMID 34573059›Full record

ArticleAntioxidants (Basel, Switzerland)2021

Selenoprotein T Protects Endothelial Cells against Lipopolysaccharide-Induced Activation and Apoptosis.

Dennis Merk, Johannes Ptok, Philipp Jakobs, Florian von Ameln, Jan Greulich, Pia Kluge, Kathrin Semperowitsch, Olaf Eckermann, Heiner Schaal, Niloofar Ale-Agha and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 15 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

12 authors at 1 institution in 1 country.

Dennis MerkEnvironmentally-Induced Cardiovascular Degeneration, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich-Heine University Düsseldorf, 40225 Düsseldorf, Germany.
Johannes PtokInstitute for Virology, Medical Faculty, University Hospital and Heinrich-Heine University Düsseldorf, 40225 Düsseldorf, Germany.
Philipp JakobsEnvironmentally-Induced Cardiovascular Degeneration, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich-Heine University Düsseldorf, 40225 Düsseldorf, Germany.
Florian von AmelnEnvironmentally-Induced Cardiovascular Degeneration, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich-Heine University Düsseldorf, Germany and IUF-Leibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.
Jan GreulichEnvironmentally-Induced Cardiovascular Degeneration, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich-Heine University Düsseldorf, Germany and IUF-Leibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.
Pia KlugeEnvironmentally-Induced Cardiovascular Degeneration, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich-Heine University Düsseldorf, 40225 Düsseldorf, Germany.
Kathrin SemperowitschEnvironmentally-Induced Cardiovascular Degeneration, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich-Heine University Düsseldorf, 40225 Düsseldorf, Germany.
Olaf EckermannEnvironmentally-Induced Cardiovascular Degeneration, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich-Heine University Düsseldorf, 40225 Düsseldorf, Germany.
Heiner SchaalInstitute for Virology, Medical Faculty, University Hospital and Heinrich-Heine University Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0000-0002-1636-4365
Niloofar Ale-AghaEnvironmentally-Induced Cardiovascular Degeneration, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich-Heine University Düsseldorf, 40225 Düsseldorf, Germany.
Joachim AltschmiedEnvironmentally-Induced Cardiovascular Degeneration, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich-Heine University Düsseldorf, 40225 Düsseldorf, Germany.
Judith HaendelerEnvironmentally-Induced Cardiovascular Degeneration, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich-Heine University Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0000-0001-8507-4540
Düsseldorf University Hospital · DE

Funding

Bayer Grant4target 2019-08-2427Deutsche Forschungsgemeinschaft IRTG1902 P1 and P2Intramural funding University of Düsseldorf 9772727
6 · The paper itself

Abstract

Sepsis is an exaggerated immune response upon infection with lipopolysaccharide (LPS) as the main causative agent. LPS-induced activation and apoptosis of endothelial cells (EC) can lead to organ dysfunction and finally organ failure. We previously demonstrated that the first twenty amino acids of the Apurinic/Apyrimidinic Endodeoxyribonuclease 1 (APEX1) are sufficient to inhibit EC apoptosis. To identify genes whose regulation by LPS is affected by this N-terminal APEX1 peptide, EC were transduced with an expression vector for the APEX1 peptide or an empty control vector and treated with LPS. Following RNA deep sequencing, genes upregulated in LPS-treated EC expressing the APEX1 peptide were identified bioinformatically. Selected candidates were validated by semi-quantitative real time PCR, a promising one was Selenoprotein T (SELENOT). For functional analyses, an expression vector for SELENOT was generated. To study the effect of SELENOT expression on LPS-induced EC activation and apoptosis, the SELENOT vector was transfected in EC. Immunostaining showed that SELENOT was expressed and localized in the ER. EC transfected with the SELENOT plasmid showed no activation and reduced apoptosis induced by LPS. SELENOT as well as APEX1(1-20) can protect EC against activation and apoptosis and could provide new therapeutic approaches in the treatment of sepsis.

Indexed as

APEX1(1-20)apoptosisendothelial cell activationlipopolysaccharideSelenoprotein T

Identifiers

PMID34573059
PMCPMC8469382
OpenAlexW3196424468

What OpenQuestion holds

Textmetadata
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.