Evidence map›Paper›PMID 27185186›Full record

ArticleCellular signalling2016

Myofibril growth during cardiac hypertrophy is regulated through dual phosphorylation and acetylation of the actin capping protein CapZ.

Ying-Hsi Lin, Chad M Warren, Jieli Li, Timothy A McKinsey, Brenda Russell

Abstract read
In one paragraph

Article in Cellular signalling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Cardiac CapZ Regulation During Acute Exercise in Female Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  4. Review
  5. Article
  6. Cytoskeletal association of ATP citrate lyase controls the mechanodynamics of macropinocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
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  15. Review
  16. Article
  17. Mechanisms of in utero cortisol effects on the newborn heart revealed by transcriptomic modeling.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
    Article
  18. Article
  19. Review
  20. Overview of the Muscle Cytoskeleton.Comprehensive Physiology · 2017
    Review
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

5 authors at 2 institutions in 1 country.

Ying-Hsi LinDepartment of Physiology and Biophysics, University of Illinois at Chicago, College of Medicine, Chicago, IL 60612-7342, United States; Department of Physiology & Biophysics, Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, IL 60612-7342, United States.
Chad M WarrenDepartment of Physiology and Biophysics, University of Illinois at Chicago, College of Medicine, Chicago, IL 60612-7342, United States; Department of Physiology & Biophysics, Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, IL 60612-7342, United States.
Jieli LiDepartment of Physiology and Biophysics, University of Illinois at Chicago, College of Medicine, Chicago, IL 60612-7342, United States; Department of Physiology & Biophysics, Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, IL 60612-7342, United States.
Timothy A McKinseyDepartment of Medicine, Division of Cardiology and Center for Fibrosis Research and Translation, University of Colorado Anschutz Medical Campus, Aurora, CO 80045-0508, United States.
Brenda RussellDepartment of Physiology and Biophysics, University of Illinois at Chicago, College of Medicine, Chicago, IL 60612-7342, United States; Department of Physiology & Biophysics, Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, IL 60612-7342, United States. Electronic address: russell@uic.edu.
University of Illinois Chicago · USUniversity of Colorado Anschutz Medical Campus · US

Funding

Sarcomeric Modifications and Progressive Cardiac MaladaptationP01HL062426 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DE TOMBE, PIETER P. · 2000 to 2020
$42.4M
Regulation of Chromatin Signaling in Heart Failure by the BRD4 Bromodomain Protein.R01HL127240 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY, SRIVASTAVA, DEEPAK · 2015 to 2022
$6.4M
Regulation of Cardiac Signaling by Class I Histone DeacetylasesR01HL116848 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY · 2013 to 2021
$3.1M
Isoform-Selective HDAC Inhibitors for Age-Associated Diastolic DysfunctionR21AG043822 · NIA · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY · 2012 to 2013
$414k
NHLBI NIH HHS P01 HL062426NHLBI NIH HHS R01 HL116848NHLBI NIH HHS R01 HL127240NIA NIH HHS R21 AG043822
6 · The paper itself

Abstract

The mechanotransduction signaling pathways initiated in heart muscle by increased mechanical loading are known to lead to long-term transcriptional changes and hypertrophy, but the rapid events for adaptation at the sarcomeric level are not fully understood. The goal of this study was to test the hypothesis that actin filament assembly during cardiomyocyte growth is regulated by post-translational modifications (PTMs) of CapZβ1. In rapidly hypertrophying neonatal rat ventricular myocytes (NRVMs) stimulated by phenylephrine (PE), two-dimensional gel electrophoresis (2DGE) of CapZβ1 revealed a shift toward more negative charge. Consistent with this, mass spectrometry identified CapZβ1 phosphorylation on serine-204 and acetylation on lysine-199, two residues which are near the actin binding surface of CapZβ1. Ectopic expression of dominant negative PKCɛ (dnPKCɛ) in NRVMs blunted the PE-induced increase in CapZ dynamics, as evidenced by the kinetic constant (Kfrap) of fluorescence recovery after photobleaching (FRAP), and concomitantly reduced phosphorylation and acetylation of CapZβ1. Furthermore, inhibition of class I histone deacetylases (HDACs) increased lysine-199 acetylation on CapZβ1, which increased Kfrap of CapZ and stimulated actin dynamics. Finally, we show that PE treatment of NRVMs results in decreased binding of HDAC3 to myofibrils, suggesting a signal-dependent mechanism for the regulation of sarcomere-associated CapZβ1 acetylation. Taken together, this dual regulation through phosphorylation and acetylation of CapZβ1 provides a novel model for the regulation of myofibril growth during cardiac hypertrophy.

Indexed as

AcetylationActinsAmino Acid SequenceAnimalsAnimals, NewbornCapZ Actin Capping ProteinCardiomegalyCell SizeHeart VentriclesHistone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesModels, BiologicalMyocytes, CardiacMyofibrilsPhenylephrineActinsCapZ Actin Capping ProteinHistone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesPhenylephrineProtein Kinase C-epsilonActin assemblyMechanotransductionProteomicsSarcomereSignaling pathways

Identifiers

PMID27185186
PMCPMC4987081
OpenAlexW2366169642

What OpenQuestion holds

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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.