Evidence map›Paper›PMID 21765055›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2011

Effects of increased systolic Ca²⁺ and phospholamban phosphorylation during β-adrenergic stimulation on Ca²⁺ transient kinetics in cardiac myocytes.

Steve R Roof, Thomas R Shannon, Paul M L Janssen, Mark T Ziolo

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 22 citations in OpenAlex.

  1. Mechanisms underlying local CaThe Journal of physiology · 2025
    Article
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  6. Cardiac Inotropic Effect of Long-Term Administration of Oral Thymoquinone.Evidence-based complementary and alternative medicine : eCAM · 2019
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Automated analysis of contractile force and Ca2+ transients in engineered heart tissue.American journal of physiology. Heart and circulatory physiology · 2014
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

4 authors at 2 institutions in 1 country.

Steve R RoofDepartment of Physiology & Cell Biology, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio 43210, USA.
Thomas R Shannon
Paul M L Janssen
Mark T Ziolo
The Ohio State University · USRush University · US

Funding

Physiology and Pathophysiology of SR Ca FluxesR01HL071893 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI SHANNON, THOMAS R · 2003 to 2011
$3.0M
NOS1/NOS3 Functional Effects on Cardiac Myocyte FunctionR01HL079283 · NHLBI · OHIO STATE UNIVERSITY · PI ZIOLO, MARK T · 2006 to 2010
$1.8M
Nitric oxide signaling in healthy and diseased cardiac myocytesK02HL094692 · NHLBI · OHIO STATE UNIVERSITY · PI ZIOLO, MARK T · 2009 to 2013
$521k
NHLBI NIH HHS K02HL-094692NHLBI NIH HHS R01HL-071893NHLBI NIH HHS R01HL-079283
6 · The paper itself

Abstract

Previous studies demonstrated higher systolic intracellular Ca(2+) concentration ([Ca(2+)](i)) amplitudes result in faster [Ca(2+)](i) decline rates, as does β-adrenergic (β-AR) stimulation. The purpose of this study is to determine the major factor responsible for the faster [Ca(2+)](i) decline rate with β-AR stimulation, the increased systolic Ca(2+) concentration levels, or phosphorylation of phospholamban. Mouse myocytes were perfused under basal conditions [1 mM extracellular Ca(2+) concentration ([Ca(2+)](o))], followed by high extracellular Ca(2+) (3 mM [Ca(2+)](o)), washout with 1 mM [Ca(2+)](o), followed by 1 μM isoproterenol (ISO) with 1 mM [Ca(2+)](o). ISO increased Ser(16) phosphorylation compared with 3 mM [Ca(2+)](o), whereas Thr(17) phosphorylation was similar. Ca(2+) transient (CaT) (fluo 4) data were obtained from matched CaT amplitudes with 3 mM [Ca(2+)](o) and ISO. [Ca(2+)](i) decline was significantly faster with ISO compared with 3 mM [Ca(2+)](o). Interestingly, the faster decline with ISO was only seen during the first 50% of the decline. CaT time to peak was significantly faster with ISO compared with 3 mM [Ca(2+)](o). A Ca(2+)/calmodulin-dependent protein kinase (CAMKII) inhibitor (KN-93) did not affect the CaT decline rates with 3 mM [Ca(2+)](o) or ISO but normalized ISO's time to peak with 3 mM [Ca(2+)](o). Thus, during β-AR stimulation, the major factor for the faster CaT decline is due to Ser(16) phosphorylation, and faster time to peak is due to CAMKII activation.

Indexed as

Adenosine TriphosphatasesAdrenergic beta-2 Receptor AgonistsAdrenergic beta-AgonistsAnimalsBenzenesulfonamidesBenzylaminesBlotting, WesternCalciumCalcium-Binding ProteinsCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium SignalingEnzyme ActivationIn Vitro TechniquesIsoproterenolKineticsMiceAdenosine TriphosphatasesAdrenergic beta-2 Receptor AgonistsAdrenergic beta-AgonistsBenzenesulfonamidesBenzylaminesCalciumCalcium-Binding ProteinsCalcium-Calmodulin-Dependent Protein Kinase Type 2IsoproterenolKN 93PhospholambanSerineSulfonamides

Identifiers

PMID21765055
PMCPMC3197371
OpenAlexW1974229149

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.