Evidence map›Paper›PMID 20008271›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2010

Phospholemman and beta-adrenergic stimulation in the heart.

JuFang Wang, Erhe Gao, Jianliang Song, Xue-Qian Zhang, Jifen Li, Walter J Koch, Amy L Tucker, Kenneth D Philipson, Tung O Chan, Arthur M Feldman and 1 more

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Methylene Blue Counteracts HCardiovascular toxicology · 2018
    Article
  5. Article
  6. Methylene blue counteracts cyanide cardiotoxicity: cellular mechanisms.Journal of applied physiology (Bethesda, Md. : 1985) · 2018
    Article
  7. Article
  8. Article
  9. Methylene blue counteracts H2S toxicity-induced cardiac depression by restoring L-type Ca channel activity.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
  10. Article
  11. Article
  12. Article
  13. Regulation of L-type calcium channel by phospholemman in cardiac myocytes.Journal of molecular and cellular cardiology · 2015
    Article
  14. Article
  15. Article
  16. Na⁺ transport in the normal and failing heart - remember the balance.Journal of molecular and cellular cardiology · 2013
    Review
  17. Article
  18. Article
  19. Article
  20. 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

11 authors at 4 institutions in 1 country.

JuFang WangDepartment of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Erhe Gao
Jianliang Song
Xue-Qian Zhang
Jifen Li
Walter J Koch
Amy L Tucker
Kenneth D Philipson
Tung O Chan
Arthur M Feldman
Joseph Y Cheung
Thomas Jefferson University · USPediatric Nephrology of Alabama · USUniversity of California, Los Angeles · USUniversity of Virginia · US

Funding

Regulation of Beta-Adrenergic Receptor Signaling by S-NitrosylationP01HL075443 · NHLBI · DUKE UNIVERSITY · PI STAMLER, JONATHAN S. · 2004 to 2019
$26.1M
Targeted Cancer Therapeutics and Heart Failure: Mechanisms and Post-injury RepairP01HL091799 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI HOUSER, STEVEN R · 2008 to 2018
$23.1M
STRUCTURE/FUNCTION OF CARDIAC SODIUM/CALCIUM EXCHANGER01HL049101 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PHILIPSON, KENNETH · 1993 to 2011
$5.8M
Molecular Biology of Cardiac Sodium-Calcium ExchangeR01HL048509 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GOLDHABER, JOSHUA I, PHILIPSON, KENNETH · 2002 to 2016
$4.7M
Targeting GRK2 in the HeartR01HL061690 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI KOCH, WALTER J. · 1998 to 2022
$4.2M
EXERCISE TRAINING IN POSTINFARCT HEARTR01HL058672 · NHLBI · WEIS CENTER FOR RESEARCH-GEISINGER CLINC · PI CHEUNG, JOSEPH Y · 1998 to 2012
$3.6M
GRK and b-Arrestin Signaling in Cardiac RegenerationR01HL085503 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI KOCH, WALTER J. · 2007 to 2015
$3.0M
Phospholemman and Cardiac ContractilityR01HL074854 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI CHEUNG, JOSEPH Y · 2005 to 2014
$2.8M
Gene Transfer and Myocardial FunctionR01HL056205 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI KOCH, WALTER J. · 1998 to 2008
$2.6M
NHLBI NIH HHS P01-HL-75443NHLBI NIH HHS P01-HL-91799NHLBI NIH HHS R01-HL-48509NHLBI NIH HHS R01-HL-49101NHLBI NIH HHS R01-HL-56205NHLBI NIH HHS R01-HL-58672NHLBI NIH HHS R01-HL-61690NHLBI NIH HHS R01-HL-74854NHLBI NIH HHS R01-HL-85503
6 · The paper itself

Abstract

Phosphorylation at serine 68 of phospholemman (PLM) in response to beta-adrenergic stimulation results in simultaneous inhibition of cardiac Na(+)/Ca(2+) exchanger NCX1 and relief of inhibition of Na(+)-K(+)-ATPase. The role of PLM in mediating beta-adrenergic effects on in vivo cardiac function was investigated with congenic PLM-knockout (KO) mice. Echocardiography showed similar ejection fraction between wild-type (WT) and PLM-KO hearts. Cardiac catheterization demonstrated higher baseline contractility (+dP/dt) but similar relaxation (-dP/dt) in PLM-KO mice. In response to isoproterenol (Iso), maximal +dP/dt was similar but maximal -dP/dt was reduced in PLM-KO mice. Dose-response curves to Iso (0.5-25 ng) for WT and PLM-KO hearts were superimposable. Maximal +dP/dt was reached 1-2 min after Iso addition and declined with time in WT but not PLM-KO hearts. In isolated myocytes paced at 2 Hz. contraction and intracellular Ca(2+) concentration ([Ca(2+)](i)) transient amplitudes and [Na(+)](i) reached maximum 2-4 min after Iso addition, followed by decline in WT but not PLM-KO myocytes. Reducing pacing frequency to 0.5 Hz resulted in much smaller increases in [Na(+)](i) and no decline in contraction and [Ca(2+)](i) transient amplitudes with time in Iso-stimulated WT and PLM-KO myocytes. Although baseline Na(+)-K(+)-ATPase current was 41% higher in PLM-KO myocytes because of increased alpha(1)- but not alpha(2)-subunit activity, resting [Na(+)](i) was similar between quiescent WT and PLM-KO myocytes. Iso increased alpha(1)-subunit current (I(alpha1)) by 73% in WT but had no effect in PLM-KO myocytes. Iso did not affect alpha(2)-subunit current (I(alpha2)) in WT and PLM-KO myocytes. In both WT and NCX1-KO hearts, PLM coimmunoprecipitated with Na(+)-K(+)-ATPase alpha(1)- and alpha(2)-subunits, indicating that association of PLM with Na(+)-K(+)-ATPase did not require NCX1. We conclude that under stressful conditions in which [Na(+)](i) was high, beta-adrenergic agonist-mediated phosphorylation of PLM resulted in time-dependent reduction in inotropy due to relief of inhibition of Na(+)-K(+)-ATPase.

Indexed as

Adrenergic beta-AgonistsAnimalsCalciumCells, CulturedHeartIsoproterenolMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutModels, AnimalMyocardial ContractionMyocardiumMyocytes, CardiacPhosphoproteinsReceptors, Adrenergic, betaAdrenergic beta-AgonistsCalciumIsoproterenolMembrane ProteinsphospholemmanPhosphoproteinsReceptors, Adrenergic, betaSodium-Calcium ExchangerSodium-Potassium-Exchanging ATPase

Identifiers

PMID20008271
PMCPMC2838560
OpenAlexW1979675289

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.