Evidence map›Paper›PMID 25260617›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2014

Actin dynamics is rapidly regulated by the PTEN and PIP2 signaling pathways leading to myocyte hypertrophy.

Jieli Li, Elaine J Tanhehco, Brenda Russell

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Spatiotemporal distribution of PTEN before directed cell migration in monolayers.In vitro cellular & developmental biology. Animal · 2024
    Article
  3. Article
  4. Review
  5. Review
  6. Courier service for phosphatidylinositol: PITPs deliver on demand.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2021
    Review
  7. Article
  8. Article
  9. PEBP1/RKIP behavior: a mirror of actin-membrane organization.Cellular and molecular life sciences : CMLS · 2020
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
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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

3 authors at 1 institution in 1 country.

Jieli LiDepartment of Physiology and Biophysics, University of Illinois at Chicago, Chicago, Illinois.
Elaine J TanhehcoDepartment of Physiology and Biophysics, University of Illinois at Chicago, Chicago, Illinois.
Brenda RussellDepartment of Physiology and Biophysics, University of Illinois at Chicago, Chicago, Illinois russell@uic.edu.
University of Illinois Chicago · US

Funding

Sarcomeric Modifications and Progressive Cardiac MaladaptationP01HL062426 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DE TOMBE, PIETER P. · 2000 to 2020
$42.4M
NHLBI NIH HHS HL-62426
6 · The paper itself

Abstract

Mature cardiac myocytes are terminally differentiated, and the heart has limited capacity to replace lost myocytes. Thus adaptation of myocyte size plays an important role in the determination of cardiac function. The hypothesis tested is that regulation of the dynamic exchange of actin leads to cardiac hypertrophy. ANG II was used as a hypertrophic stimulant in mouse heart and neonatal rat ventricular myocytes (NRVMs) in culture for assessment of a mechanism for regulation of actin dynamics by phosphatidylinositol 4,5-bisphosphate (PIP2). Actin dynamics in NRVMs rapidly increased in a PIP2-dependent manner, measured by imaging and fluorescence recovery after photobleaching (FRAP). A significant increase in PIP2 levels was found by immunoblotting in both adult mouse heart tissue and cultured NRVMs. Inhibition of phosphatase and tensin homolog (PTEN) in NRVMs markedly blunted ANG II-induced increases in actin dynamics, the PIP2 level, and cell size. Furthermore, PTEN activity was dramatically upregulated in ANG II-treated NRVMs but downregulated when PTEN inhibitors were used. The time course of the rise in the PIP2 level was inversely related to the fall in the PIP3 level, which was significant by 30 min in ANG II-treated NRVMs. However, significant translocation of PTEN to the plasma membrane occurred by 10 min, suggesting a crucial initial step for PTEN for the cellular responses to ANG II. In conclusion, PTEN and PIP2 signaling may play an important role in myocyte hypertrophy by the regulation of actin filament dynamics, which is induced by ANG II stimulation.

Indexed as

ActinsAngiotensin IIAnimalsCardiomegalyCell SizeEnzyme ActivationMiceMice, Inbred C57BLMyocytes, CardiacPhosphatidylinositol 4,5-DiphosphatePhosphatidylinositol PhosphatesPTEN PhosphohydrolaseRatsRats, Sprague-DawleySignal TransductionSubcellular FractionsActinsAngiotensin IIphosphatidylinositol 3,4,5-triphosphatePhosphatidylinositol 4,5-DiphosphatePhosphatidylinositol PhosphatesPTEN PhosphohydrolaseG protein receptorslipid signalingmembrane translocationsarcomere remodeling

Identifiers

PMID25260617
PMCPMC4255012
OpenAlexW2020024864

What OpenQuestion holds

Textmetadata
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.