Evidence map›Paper›PMID 20159036›Full record

ArticleCellular signalling2010

Involvement of the MEKK1 signaling pathway in the regulation of epicardial cell behavior by hyaluronan.

Evisabel A Craig, Patti Parker, Anita F Austin, Joey V Barnett, Todd D Camenisch

Abstract read
In one paragraph

Article in Cellular signalling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Epicardium-myocardium crosstalk orchestrates heart development.Frontiers in cell and developmental biology · 2025
    Review
  3. CCBE1 Is Essential for Epicardial Function during Myocardium Development.International journal of molecular sciences · 2022
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Extracellular matrix and heart development.Birth defects research. Part A, Clinical and molecular teratology · 2011
    Review
  17. 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

5 authors at 2 institutions in 1 country.

Evisabel A CraigDepartment of Pharmacology and Toxicology, The University of Arizona, Tucson, Arizona, USA.
Patti Parker
Anita F Austin
Joey V Barnett
Todd D Camenisch
University of Arizona · USVanderbilt University Medical Center · US

Funding

Type III Transforming Growth Factor beta Receptor in Coronary Vessel DevelopmentR01HL085708 · NHLBI · VANDERBILT UNIVERSITY · PI BARNETT, JOEY VICTOR · 2008 to 2011
$1.7M
Hyaluronan and erbBs regulate cardiac valve formationR01HL077493 · NHLBI · UNIVERSITY OF ARIZONA · PI CAMENISCH, TODD D · 2004 to 2007
$1.6M
Mechanisms for Has2 activation and hyaluronan-mediated cellular invasionF31HL095155 · NHLBI · UNIVERSITY OF ARIZONA · PI CRAIG, EVISABEL A · 2009 to 2010
$59k
NHLBI NIH HHS 1F31HL095155NHLBI NIH HHS F31 HL095155NHLBI NIH HHS HL077493NHLBI NIH HHS HL085708NHLBI NIH HHS R01 HL077493NHLBI NIH HHS R01 HL085708
6 · The paper itself

Abstract

During embryonic development, cells comprising the outermost layer of the heart or epicardium play a critical role in the formation of the coronary vasculature. Thus, uncovering the molecular mechanisms that govern epicardial cell behavior is imperative to better understand the etiology of cardiovascular diseases. In this study, we investigated the function of hyaluronan (HA), a major component of the extracellular matrix, in the modulation of epicardial signaling. We show that stimulation of epicardial cells with high molecular weight HA (HMW-HA) promotes the association of MEKK1 with the HA receptor CD44 and induces MEKK1 phosphorylation. This leads to the activation of two distinct pathways, one ERK-dependent and another NFkappaB-dependent. Furthermore, HMW-HA stimulates epicardial cells to differentiate and invade, as suggested by increased vimentin expression and enhanced invasion through a collagen matrix. Blockade of CD44, transfection with a kinase-inactive MEKK1 construct or the use of ERK1/2 and NFkappaB inhibitors significantly abrogates the invasive response to HMW-HA. Together, these findings suggest an important role for HA in the regulation of epicardial cell fate via activation of MEKK1 signaling cascades.

Indexed as

MAP Kinase Signaling SystemAnimalsCell DifferentiationCell LineCell MovementExtracellular Signal-Regulated MAP KinasesHyaluronan ReceptorsHyaluronic AcidMAP Kinase Kinase Kinase 1MiceMice, TransgenicNF-kappa BPericardiumSerum Response ElementSnail Family Transcription FactorsTranscription FactorsExtracellular Signal-Regulated MAP KinasesHyaluronan ReceptorsHyaluronic AcidMAP Kinase Kinase Kinase 1NF-kappa BSnail Family Transcription FactorsTranscription Factors

Identifiers

PMID20159036
PMCPMC2846756
OpenAlexW2052589908

What OpenQuestion holds

Textmetadata
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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.