Evidence map›Paper›PMID 30281646›Full record

ArticlePloS one2018

Loss of Ccbe1 affects cardiac-specification and cardiomyocyte differentiation in mouse embryonic stem cells.

Oriol Bover, Tiago Justo, Paulo N G Pereira, João Facucho-Oliveira, José M Inácio, José S Ramalho, Ibrahim J Domian, José António Belo

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.1field-weighted citation impact, top 51% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. CCBE1 in Cardiac Development and Disease.Frontiers in genetics · 2022
    Review
  4. 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 3 institutions in 2 countries.

Oriol BoverStem Cells and Development Laboratory, CEDOC, Chronic Diseases Research Centre, NOVA Medical School|Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, Lisboa, Portugal.
Tiago JustoStem Cells and Development Laboratory, CEDOC, Chronic Diseases Research Centre, NOVA Medical School|Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, Lisboa, Portugal.
Paulo N G PereiraStem Cells and Development Laboratory, CEDOC, Chronic Diseases Research Centre, NOVA Medical School|Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, Lisboa, Portugal.
João Facucho-OliveiraCenter for Biomedical Research, Campus de Gambelas, University of Algarve, Faro, Portugal.
José M InácioStem Cells and Development Laboratory, CEDOC, Chronic Diseases Research Centre, NOVA Medical School|Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, Lisboa, Portugal.
José S RamalhoCEDOC, Chronic Diseases Research Centre, NOVA Medical School|Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, Lisboa, Portugal.ORCID 0000-0002-1927-164X
Ibrahim J DomianCardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts, United States of America.
José António BeloStem Cells and Development Laboratory, CEDOC, Chronic Diseases Research Centre, NOVA Medical School|Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, Lisboa, Portugal.ORCID 0000-0001-7384-0949
Universidade Nova de Lisboa · PTUniversity of Algarve · PTMassachusetts General Hospital · US

Funding

The Role of Cardiomyocyte Polarity in Cardiac MorphogenesisR01HL130391 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI DOMIAN, IBRAHIM J · 2016 to 2019
$1.7M
NHLBI NIH HHS R01 HL130391
6 · The paper itself

Abstract

Understanding the molecular pathways regulating cardiogenesis is crucial for the early diagnosis of heart diseases and improvement of cardiovascular disease. During normal mammalian cardiac development, collagen and calcium-binding EGF domain-1 (Ccbe1) is expressed in the first and second heart field progenitors as well as in the proepicardium, but its role in early cardiac commitment remains unknown. Here we demonstrate that during mouse embryonic stem cell (ESC) differentiation Ccbe1 is upregulated upon emergence of Isl1- and Nkx2.5- positive cardiac progenitors. Ccbe1 is markedly enriched in Isl1-positive cardiac progenitors isolated from ESCs differentiating in vitro or embryonic hearts developing in vivo. Disruption of Ccbe1 activity by shRNA knockdown or blockade with a neutralizing antibody results in impaired differentiation of embryonic stem cells along the cardiac mesoderm lineage resulting in a decreased expression of mature cardiomyocyte markers. In addition, knockdown of Ccbe1 leads to smaller embryoid bodies. Collectively, our results show that CCBE1 is essential for the commitment of cardiac mesoderm and consequently, for the formation of cardiac myocytes in differentiating mouse ESCs.

Indexed as

AnimalsCalcium-Binding ProteinsCell DifferentiationCells, CulturedGene Expression Regulation, DevelopmentalGene Knockdown TechniquesHeartHomeobox Protein Nkx-2.5LIM-Homeodomain ProteinsMiceMice, TransgenicMouse Embryonic Stem CellsMyocardiumMyocytes, CardiacRNA, Small InterferingTranscription FactorsCalcium-Binding ProteinsCcbe1 protein, mouseHomeobox Protein Nkx-2.5insulin gene enhancer binding protein Isl-1LIM-Homeodomain ProteinsNkx2-5 protein, mouseRNA, Small InterferingTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID30281646
PMCPMC6169972
OpenAlexW2895309425

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.