Evidence map›Paper›PMID 22465692›Full record

ArticleJournal of molecular and cellular cardiology2012

Excitation-contraction coupling in ventricular myocytes is enhanced by paracrine signaling from mesenchymal stem cells.

J DeSantiago, D J Bare, I Semenov, R D Minshall, D L Geenen, B M Wolska, K Banach

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

J DeSantiagoCenter for Cardiovascular Research, Department of Medicine, Section of Cardiology, University of Illinois at Chicago, Chicago, IL 60612, USA. jdesant@uic.edu
D J Bare
I Semenov
R D Minshall
D L Geenen
B M Wolska
K Banach
University of Illinois Chicago · USThe University of Texas Health Science Center at San Antonio · US

Funding

PREPARATION AND DISTRUBUTION OF ADULT STEM CELLS: HUMAN &RODENTP40RR017447 · NCRR · TULANE UNIVERSITY OF LOUISIANA · PI PROCKOP, DARWIN JOHNSON · 2003 to 2011
$8.9M
Troponin Mudulation in Heart FailureR01HL064035 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SOLARO, R JOHN, WOLSKA, BEATA M. · 2000 to 2013
$4.7M
Src Regulation of Lung Endothelial Barrier FunctionR01HL071626 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MINSHALL, RICHARD D · 2003 to 2011
$2.4M
Embryonic Stem Cell Derived Biological Pacemaker for the HeartR01HL089617 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI BANACH, KATHRIN · 2007 to 2011
$2.0M
Control of Cardiac Function by Calcium and MyofilamentsR01HL079032 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI WOLSKA, BEATA M. · 2005 to 2008
$1.3M
NCRR NIH HHS P40 RR017447NCRR NIH HHS P40RR017447NHLBI NIH HHS HL064035NHLBI NIH HHS HL071626NHLBI NIH HHS HL089617NHLBI NIH HHS HL089617-03S1NHLBI NIH HHS HL79032NHLBI NIH HHS R01 HL064035NHLBI NIH HHS R01 HL071626NHLBI NIH HHS R01 HL079032NHLBI NIH HHS R01 HL089617
6 · The paper itself

Abstract

In clinical trials mesenchymal stem cells (MSCs) are transplanted into cardiac ischemic regions to decrease infarct size and improve contractility. However, the mechanism and time course of MSC-mediated cardioprotection are incompletely understood. We tested the hypothesis that paracrine signaling by MSCs promotes changes in cardiac excitation-contraction (EC) coupling that protects myocytes from cell death and enhances contractility. Isolated mouse ventricular myocytes (VMs) were treated with control tyrode, MSC conditioned-tyrode (ConT) or co-cultured with MSCs. The Ca handling properties of VMs were monitored by laser scanning confocal microscopy and whole cell voltage clamp. ConT superfusion of VMs resulted in a time dependent increase of the Ca transient amplitude (ConT(15min): ΔF/F(0)=3.52±0.38, n=14; Ctrl(15min): ΔF/F(0)=2.41±0.35, n=14) and acceleration of the Ca transient decay (τ: ConT: 269±18ms n=14; vs. Ctrl: 315±57ms, n=14). Voltage clamp recordings confirmed a ConT induced increase in I(Ca,L) (ConT: -5.9±0.5 pA/pF n=11; vs. Ctrl: -4.04±0.3 pA/pF, n=12). The change of τ resulted from increased SERCA activity. Changes in the Ca transient amplitude and τ were prevented by the PI3K inhibitors Wortmannin (100nmol/L) and LY294002 (10μmol/L) and the Akt inhibitor V (20μmol/L) indicating regulation through PI3K signal transduction and Akt activation which was confirmed by western blotting. A change in τ was also prevented in eNOS(-/-) myocytes or by inhibition of eNOS suggesting an NO mediated regulation of SERCA activity. Since paracrine signaling further resulted in increased survival of VMs we propose that the Akt induced change in Ca signaling is also a mechanism by which MSCs mediate an anti-apoptotic effect.

Indexed as

AnimalsCalciumCells, CulturedExcitation Contraction CouplingHeart VentriclesMesenchymal Stem CellsMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacParacrine CommunicationProto-Oncogene Proteins c-aktSignal TransductionCalciumProto-Oncogene Proteins c-akt

Identifiers

PMID22465692
PMCPMC3570146
OpenAlexW2081988898

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.