Evidence map›Paper›PMID 31425567›Full record

ArticlePloS one2019

Overexpression of protein phosphatase 5 in the mouse heart: Reduced contractility but increased stress tolerance - Two sides of the same coin?

Ulrich Gergs, Tina Jahn, Franziska Werner, Carolin Köhler, Friedrich Köpp, Claudia Großmann, Joachim Neumann

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Mechanisms of systolic heart failure in PP2CxPP5 double transgenic mice.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Article
  2. Article
  3. Cardiovascular effects of bufotenin on human 5-HTNaunyn-Schmiedeberg's archives of pharmacology · 2023
    Article
  4. Article
  5. Article
  6. Article
  7. Functional interaction of HNaunyn-Schmiedeberg's archives of pharmacology · 2021
    Article
  8. Article
  9. Influence of Serotonin 5-HTBiomedicines · 2021
    Article
  10. ACTH(6-9)PGP Peptide Protects SH-SY5Y Cells from HMolecules (Basel, Switzerland) · 2021
    Article
  11. Article
  12. Review
  13. Article
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

7 authors at 1 institution in 1 country.

Ulrich GergsInstitut für Pharmakologie und Toxikologie, Medizinische Fakultät, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Germany.ORCID 0000-0001-6986-485X
Tina JahnInstitut für Pharmakologie und Toxikologie, Medizinische Fakultät, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Germany.
Franziska WernerInstitut für Pharmakologie und Toxikologie, Medizinische Fakultät, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Germany.
Carolin KöhlerInstitut für Pharmakologie und Toxikologie, Medizinische Fakultät, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Germany.
Friedrich KöppInstitut für Pharmakologie und Toxikologie, Medizinische Fakultät, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Germany.
Claudia GroßmannJulius-Bernstein-Institut für Physiologie, Medizinische Fakultät, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Germany.
Joachim NeumannInstitut für Pharmakologie und Toxikologie, Medizinische Fakultät, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Germany.
Martin Luther University Halle-Wittenberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathophysiological mechanisms of sepsis-induced cardiac dysfunction are largely unknown. The Toll-like receptor 4 (TLR4) is expressed in cardiac myocytes and is involved in bacterial endotoxin-mediated inflammatory disorders. TLR4 signaling leads to activation of the nuclear factor kappa B followed by increased expression of cytokines. Several protein phosphatases including PP2Cβ, PP2A or PP1 are known to act as regulators of this signaling pathway. Here, we examined the role of PP5 for the inflammatory response to the bacterial endotoxin lipopolysaccharide in the heart using a transgenic mouse model with cardiac myocyte directed overexpression of PP5. In these transgenic mice, basal cardiac contractility was reduced, in vivo as well as in vitro, but LPS-induced cardiac dysfunction was less pronounced compared to wild type mice. Quantitative RT-PCR suggested an attenuated NF-κB signaling in the heart and cardiac expression of heat shock protein 25 (HSP25) was increased in PP5 transgenic mice. From our data we assume that PP5 increases stress tolerance of cardiac myocytes by downregulation of NF-κB signaling and upregulation of HSP25 expression.

Indexed as

AnimalsDisease Models, AnimalDown-RegulationEchocardiographyFemaleHeart FailureHeat-Shock ProteinsHumansIsolated Heart PreparationLipopolysaccharidesMaleMiceMice, TransgenicMolecular ChaperonesMyocardial ContractionMyocytes, CardiacHeat-Shock ProteinsHsbp1 protein, mouseLipopolysaccharidesMolecular ChaperonesNF-kappa BNuclear ProteinsPhosphoprotein Phosphatasesprotein phosphatase 5Tlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID31425567
PMCPMC6699691
OpenAlexW2969568884

What OpenQuestion holds

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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.