Evidence map›Paper›PMID 29066438›Full record

ArticleJournal of the American Heart Association2017

Polo-Like Kinase 2 is Dynamically Regulated to Coordinate Proliferation and Early Lineage Specification Downstream of Yes-Associated Protein 1 in Cardiac Progenitor Cells.

Michika Mochizuki, Vera Lorenz, Robert Ivanek, Giacomo Della Verde, Emanuele Gaudiello, Anna Marsano, Otmar Pfister, Gabriela M Kuster

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

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  5. Emerging Antiarrhythmic Drugs for Atrial Fibrillation.International journal of molecular sciences · 2022
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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

8 authors at 2 institutions in 1 country.

Michika MochizukiDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland.
Vera LorenzDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland.
Robert IvanekDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland.
Giacomo Della VerdeDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland.
Emanuele GaudielloDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland.
Anna MarsanoDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland.
Otmar PfisterDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland.
Gabriela M KusterDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland gabriela.kuster@usb.ch.
University of Basel · CHUniversity Hospital of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent studies suggest that adult cardiac progenitor cells (CPCs) can produce new cardiac cells. Such cell formation requires an intricate coordination of progenitor cell proliferation and commitment, but the molecular cues responsible for this regulation in CPCs are ill defined. METHODS AND

resultsExtracellular matrix components are important instructors of cell fate. Using laminin and fibronectin, we induced two slightly distinct CPC phenotypes differing in proliferation rate and commitment status and analyzed the early transcriptomic response to CPC adhesion (<2 hours). Ninety-four genes were differentially regulated on laminin versus fibronectin, consisting of mostly downregulated genes that were enriched for Yes-associated protein (YAP) conserved signature and TEA domain family member 1 (TEAD1)-related genes. This early gene regulation was preceded by the rapid cytosolic sequestration and degradation of YAP on laminin. Among the most strongly regulated genes was polo-like kinase 2 (

conclusionsPlk2 acts as coordinator of cell proliferation and early lineage commitment in CPCs. The rapid downregulation of Plk2 on YAP inactivation marks a switch towards enhanced commitment and facilitated differentiation. These findings link early gene regulation to cell fate and provide novel insights into how CPC proliferation and differentiation are orchestrated.

Indexed as

Cell LineageCell ProliferationAdaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsCell AdhesionCell Cycle ProteinsCell DifferentiationCells, CulturedCoculture TechniquesEndothelial Progenitor CellsFibronectinsGene Expression Regulation, DevelopmentalLamininMice, TransgenicMyocytes, CardiacAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCell Cycle ProteinsFibronectinsLamininPhosphoproteinsPlk2 protein, ratProtein Serine-Threonine Kinasesserum-inducible kinaseYap1 protein, mouseYap1 protein, ratYAP-Signaling Proteinscardiac progenitor cellscell fateextracellular matrixpolo‐like kinase 2Yes‐associated protein

Identifiers

PMID29066438
PMCPMC5721832
OpenAlexW2766680473

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.