Evidence map›Paper›PMID 19605361›Full record

ArticleThe Journal of biological chemistry2009

MEK5/ERK5 signaling modulates endothelial cell migration and focal contact turnover.

Désirée Spiering, Mirco Schmolke, Nils Ohnesorge, Marc Schmidt, Matthias Goebeler, Joachim Wegener, Viktor Wixler, Stephan Ludwig

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The MEK5/ERK5 Pathway in Health and Disease.International journal of molecular sciences · 2021
    Review
  5. Review
  6. MK2 contributes to tumor progression by promoting M2 macrophage polarization and tumor angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. ERK5 Mediated Signalling in Diabetic Retinopathy.Medical hypothesis, discovery & innovation ophthalmology journal · 2015
    Review
  14. Characterization of extracellular signal-regulated kinase 5 levels in human umbilical vein endothelial cells exposed to disturbed and uniform flow.The International journal of angiology : official publication of the International College of Angiology, Inc · 2014
    Article
  15. Article
  16. Article
  17. Article
  18. 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

8 authors at 4 institutions in 1 country.

Désirée SpieringInstitute of Molecular Virology (IMV), Center of Molecular Biology of Inflammation (ZMBE), and Interdisciplinary Center of Medical Research (IZKF), Universitaetsklinikum Muenster, 48149 Muenster, Germany.
Mirco Schmolke
Nils Ohnesorge
Marc Schmidt
Matthias Goebeler
Joachim Wegener
Viktor Wixler
Stephan Ludwig
Institute of Molecular Biology · DEUniversity Medical Centre Mannheim · DEUniversity Hospital Heidelberg · DEUniversity of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The formation of new blood vessels from pre-existing ones requires highly coordinated restructuring of endothelial cells (EC) and the surrounding extracellular matrix. Directed EC migration is a central step in this process and depends on cellular signaling cascades that initiate and control the structural rearrangements. On the basis of earlier findings that ERK5 deficiency in mouse EC results in massive defects in vessel architecture, we focused on the impact of the MEK5/ERK5 signaling pathway on EC migration. Using a retroviral gene transfer approach, we found that constitutive activation of MEK5/ERK5 signaling strongly inhibits EC migration and results in massive morphological changes. The area covered by spread EC was dramatically enlarged, accompanied by an increase in focal contacts and altered organization of actin filaments. Consequently, cells were more rigid and show reduced motility. This phenotype was most likely based on decreased focal contact turnover caused by reduced expression of p130Cas, a key player in directed cell migration. We demonstrate for the first time that ERK5 signaling not only is involved in EC survival and stress response but also controls migration and morphology of EC.

Indexed as

Cell MovementCells, CulturedCell SurvivalEndothelial CellsHumansMAP Kinase Kinase 5MAP Kinase Signaling SystemMitogen-Activated Protein Kinase 7Models, BiologicalNeovascularization, PathologicPhenotypeSignal TransductionTransfectionWound HealingMAP Kinase Kinase 5Mitogen-Activated Protein Kinase 7

Identifiers

PMID19605361
PMCPMC2757201
OpenAlexW1975697750

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.