Evidence map›Paper›PMID 19066628›Full record

ArticlePloS one2008

Enhanced proliferation of monolayer cultures of embryonic stem (ES) cell-derived cardiomyocytes following acute loss of retinoblastoma.

Satoshi Yamanaka, Ihor Zahanich, Robert P Wersto, Kenneth R Boheler

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2008. 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
1.1field-weighted citation impact, top 23% 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, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Reprogramming for cardiac regeneration.Global cardiology science & practice · 2014
    Review
  10. Article
  11. Article
  12. Article
  13. Molecular mechanisms of cardiomyocyte aging.Clinical science (London, England : 1979) · 2011
    Review
  14. Article
  15. Article
  16. Article
  17. Proliferation of mouse embryonic stem cell progeny and the spontaneous contractile activity of cardiomyocytes are affected by microtopography.Developmental dynamics : an official publication of the American Association of Anatomists · 2009
    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

4 authors at 1 institution in 1 country.

Satoshi YamanakaLaboratory of Cardiovascular Science, National Institute on Aging, Baltimore, Maryland, USA.
Ihor Zahanich
Robert P Wersto
Kenneth R Boheler
National Institute on Aging · US

Funding

Flow Cytometry Laboratory (Scientific Core)ZICAG000618 · NIA · NATIONAL INSTITUTE ON AGING · PI WENG, NAN-PING PETER · 2009 to 2025
$9.5M
Embryonic Stem Cell Derived Cardiac MyocytesZIAAG000849 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHELER, KENNETH · 2009 to 2012
$2.3M
EXCITATION/CONTRACTION COUPLING--IN VITRO DIFFERENTIATED CARDIAC MYOCYTESZ01AG000849 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHELER, KENNETH R · 1997 to 2008
$1.6M
Flow Cytometry Laboratory (Scientific Core)Z01AG000618 · NIA · NATIONAL INSTITUTE ON AGING · PI WERSTO, ROBERT · 2008 to 2008
$763k
6 · The paper itself

Abstract

backgroundCardiomyocyte (CM) cell cycle analysis has been impeded because of a reliance on primary neonatal cultures of poorly proliferating cells or chronic transgenic animal models with innate compensatory mechanisms. METHODOLOGY/PRINCIPAL

findingsWe describe an in vitro model consisting of monolayer cultures of highly proliferative embryonic stem (ES) cell-derived CM. Following induction with ascorbate and selection with puromycin, early CM cultures are >98% pure, and at least 85% of the cells actively proliferate. During the proliferative stage, cells express high levels of E2F3a, B-Myb and phosphorylated forms of retinoblastoma (Rb), but with continued cultivation, cells stop dividing and mature functionally. This developmental transition is characterized by a switch from slow skeletal to cardiac TnI, an increase in binucleation, cardiac calsequestrin and hypophosphorylated Rb, a decrease in E2F3, B-Myb and atrial natriuretic factor, and the establishment of a more negative resting membrane potential. Although previous publications suggested that Rb was not necessary for cell cycle control in heart, we find following acute knockdown of Rb that this factor actively regulates progression through the G1 checkpoint and that its loss promotes proliferation at the expense of CM maturation. CONCLUSIONS/SIGNIFICANCE: We have established a unique model system for studying cardiac cell cycle progression, and show in contrast to previous reports that Rb actively regulates both cell cycle progression through the G1 checkpoint and maturation of heart cells. We conclude that this in vitro model will facilitate the analysis of cell cycle control mechanisms of CMs.

Indexed as

AnimalsApoptosisCell LineCell ProliferationCell SeparationDrug Resistance, MicrobialElectrophysiological PhenomenaEmbryonic Stem CellsG1 PhaseMyocytes, CardiacPuromycinRatsRetinoblastoma ProteinSodium-Calcium ExchangerS PhasePuromycinRetinoblastoma ProteinSodium-Calcium Exchangersodium-calcium exchanger 1

Identifiers

PMID19066628
PMCPMC2588539
OpenAlexW2093412381

What OpenQuestion holds

Textmetadata
LicenceCC0
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.