Evidence map›Paper›PMID 31645612›Full record

ArticleScientific reports2019

Proteasome activator PA200 regulates myofibroblast differentiation.

Vanessa Welk, Thomas Meul, Christina Lukas, Ilona E Kammerl, Shrikant R Mulay, Andrea C Schamberger, Nora Semren, Isis E Fernandez, Hans-Joachim Anders, Andreas Günther and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Bortezomib Inhibits Lung Fibrosis and Fibroblast Activation without Proteasome Inhibition.American journal of respiratory cell and molecular biology · 2022
    Article
  8. Article
  9. Review
  10. 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

14 authors at 3 institutions in 2 countries.

Vanessa WelkComprehensive Pneumology Center (CPC), University Hospital of the Ludwig-Maximilians-University (LMU) and Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Max-Lebsche Platz 31, 81377, Munich, Germany.
Thomas MeulComprehensive Pneumology Center (CPC), University Hospital of the Ludwig-Maximilians-University (LMU) and Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Max-Lebsche Platz 31, 81377, Munich, Germany.
Christina LukasComprehensive Pneumology Center (CPC), University Hospital of the Ludwig-Maximilians-University (LMU) and Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Max-Lebsche Platz 31, 81377, Munich, Germany.
Ilona E KammerlComprehensive Pneumology Center (CPC), University Hospital of the Ludwig-Maximilians-University (LMU) and Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Max-Lebsche Platz 31, 81377, Munich, Germany.
Shrikant R MulayDivision of Nephrology, Medizinische Klinik und Poliklinik IV, Klinikum der Universität, Ziemssenstraße 1, 80336, Munich, Germany.ORCID http://orcid.org/0000-0003-4261-445X
Andrea C SchambergerComprehensive Pneumology Center (CPC), University Hospital of the Ludwig-Maximilians-University (LMU) and Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Max-Lebsche Platz 31, 81377, Munich, Germany.
Nora SemrenComprehensive Pneumology Center (CPC), University Hospital of the Ludwig-Maximilians-University (LMU) and Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Max-Lebsche Platz 31, 81377, Munich, Germany.
Isis E FernandezComprehensive Pneumology Center (CPC), University Hospital of the Ludwig-Maximilians-University (LMU) and Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Max-Lebsche Platz 31, 81377, Munich, Germany.
Hans-Joachim AndersDivision of Nephrology, Medizinische Klinik und Poliklinik IV, Klinikum der Universität, Ziemssenstraße 1, 80336, Munich, Germany.
Andreas GüntherDepartment of Internal Medicine, Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Member of the German Center for Lung Research (DZL), Giessen, Germany.ORCID http://orcid.org/0000-0002-2187-0975
Jürgen BehrComprehensive Pneumology Center (CPC), University Hospital of the Ludwig-Maximilians-University (LMU) and Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Max-Lebsche Platz 31, 81377, Munich, Germany.
Oliver EickelbergComprehensive Pneumology Center (CPC), University Hospital of the Ludwig-Maximilians-University (LMU) and Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Max-Lebsche Platz 31, 81377, Munich, Germany.
Martina KorfeiDepartment of Internal Medicine, Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Member of the German Center for Lung Research (DZL), Giessen, Germany.ORCID http://orcid.org/0000-0001-8177-2085
Silke MeinersComprehensive Pneumology Center (CPC), University Hospital of the Ludwig-Maximilians-University (LMU) and Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Max-Lebsche Platz 31, 81377, Munich, Germany. silke.meiners@helmholtz-muenchen.de.
Helmholtz Zentrum München · DEJustus-Liebig-Universität Gießen · DELMU Klinikum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The proteasome is essential for the selective degradation of most cellular proteins and is fine-tuned according to cellular needs. Proteasome activators serve as building blocks to adjust protein turnover in cell growth and differentiation. Understanding the cellular function of proteasome activation in more detail offers a new strategy for therapeutic targeting of proteasomal protein breakdown in disease. The role of the proteasome activator PA200 in cell function and its regulation in disease is unknown. In this study, we investigated the function of PA200 in myofibroblast differentiation and fibrotic tissue remodeling. PA200 was upregulated in hyperplastic basal cells and myofibroblasts of fibrotic lungs from patients with idiopathic pulmonary fibrosis. Increased expression of PA200 and enhanced formation of PA200-proteasome complexes was also evident in experimental fibrosis of the lung and kidney in vivo and in activated primary human myofibroblasts of the lung in vitro. Transient silencing and overexpression revealed that PA200 functions as a negative regulator of myofibroblast differentiation of human but not mouse cells. Our data thus suggest an unexpected and important role for PA200 in adjusting myofibroblast activation in response to pro-fibrotic stimuli, which fails in idiopathic pulmonary fibrosis.

Indexed as

AdultAnimalsCell DifferentiationCells, CulturedFemaleFibrosisHumansIdiopathic Pulmonary FibrosisKidneyLungMaleMiceMice, Inbred C57BLMiddle AgedMyofibroblastsNuclear ProteinsNuclear ProteinsPa200 protein, mouseProteasome Endopeptidase ComplexPSME4 protein, humanTransforming Growth Factor beta

Identifiers

PMID31645612
PMCPMC6811633
OpenAlexW2982187559

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.