Evidence map›Paper›PMID 21047517›Full record

ArticleJournal of molecular and cellular cardiology2011

Modulation of human embryonic stem cell-derived cardiomyocyte growth: a testbed for studying human cardiac hypertrophy?

Gábor Földes, Maxime Mioulane, Jamie S Wright, Alexander Q Liu, Pavel Novak, Béla Merkely, Julia Gorelik, Michael D Schneider, Nadire N Ali, Sian E Harding

Open access · bronzeAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

73 citing papers in PubMed, 128 citations in OpenAlex.

  1. Article
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  4. Review
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  6. Review
  7. Article
  8. Sympathetic Neurons Regulate Cardiomyocyte Maturation in Culture.Frontiers in cell and developmental biology · 2022
    Article
  9. Review
  10. Silencing ofInternational journal of molecular sciences · 2021
    Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Human Cell Modeling for Cardiovascular Diseases.International journal of molecular sciences · 2020
    Review
  18. Article
  19. Review
  20. Article

13 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 2 countries.

Gábor FöldesNational Heart and Lung Institute, Imperial College London, London, UK. g.foldes@imperial.ac.uk
Maxime Mioulane
Jamie S Wright
Alexander Q Liu
Pavel Novak
Béla Merkely
Julia Gorelik
Michael D Schneider
Nadire N Ali
Sian E Harding
Imperial College London · GBSemmelweis University · HU

Funding

Biotechnology and Biological Sciences Research Council BB/D011027/1British Heart Foundation RG/08/007/25296Medical Research Council G0901467National Centre for the Replacement, Refinement and Reduction of Animals in Research G0600373/1National Centre for the Replacement, Refinement and Reduction of Animals in Research G1000035/1Wellcome Trust
6 · The paper itself

Abstract

Human embryonic stem cell-derived cardiomyocytes (hESC-CM) are being developed for tissue repair and as a model system for cardiac physiology and pathophysiology. However, the signaling requirements of their growth have not yet been fully characterized. We showed that hESC-CM retain their capacity for increase in size in long-term culture. Exposing hESC-CM to hypertrophic stimuli such as equiaxial cyclic stretch, angiotensin II, and phenylephrine (PE) increased cell size and volume, percentage of hESC-CM with organized sarcomeres, levels of ANF, and cytoskeletal assembly. PE effects on cell size were separable from those on cell cycle. Changes in cell size by PE were completely inhibited by p38-MAPK, calcineurin/FKBP, and mTOR blockers. p38-MAPK and calcineurin were also implicated in basal cell growth. Inhibitors of ERK, JNK, and CaMK II partially reduced PE effects; PKG or GSK3β inhibitors had no effect. The role of p38-MAPK was confirmed by an additional pharmacological inhibitor and adenoviral infection of hESC-CM with a dominant-inhibitory form of p38-MAPK. Infection of hESC-CM with constitutively active upstream MAP2K3b resulted in an increased cell size, sarcomere and cytoskeletal assembly, elongation of the cells, and induction of ANF mRNA levels. siRNA knockdown of p38-MAPK inhibited PE-induced effects on cell size. These results reveal an important role for active protein kinase signaling in hESC-CM growth and hypertrophy, with potential implications for hESC-CM as a novel in vitro test system. This article is part of a special issue entitled, "Cardiovascular Stem Cells Revisited".

Indexed as

Angiotensin IICardiomegalyCell CycleCell DifferentiationCell LineCell ProliferationCells, CulturedCell SizeEmbryonic Stem CellsGene Expression RegulationHumansMAP Kinase Kinase 3Myocytes, Cardiacp38 Mitogen-Activated Protein KinasesPhenylephrineProtein Kinase InhibitorsAngiotensin IIMAP2K3 protein, humanMAP Kinase Kinase 3p38 Mitogen-Activated Protein KinasesPhenylephrineProtein Kinase InhibitorsVasoconstrictor Agents

Identifiers

PMID21047517
PMCPMC3034871
OpenAlexW2084834807

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.