Evidence map›Paper›PMID 23614555›Full record

ArticleStem cells and development2013

Ischemia/Reperfusion injury protection by mesenchymal stem cell derived antioxidant capacity.

Jaime DeSantiago, Dan J Bare, Kathrin Banach

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cells and development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Mesenchymal Stem Cells and Their Exocytotic Vesicles.International journal of molecular sciences · 2023
    Review
  5. Review
  6. Review
  7. The human amniotic fluid stem cell secretome triggers intracellular CaJournal of cellular and molecular medicine · 2021
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. 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

3 authors at 1 institution in 1 country.

Jaime DeSantiagoSection of Cardiology, Department of Medicine, Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, Illinois 60612-7323, USA.
Dan J Bare
Kathrin Banach
University of Illinois Chicago · US

Funding

Embryonic Stem Cell Derived Biological Pacemaker for the HeartR01HL089617 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI BANACH, KATHRIN · 2007 to 2011
$2.0M
NHLBI NIH HHS HL089617NHLBI NIH HHS HL089617-03S1NHLBI NIH HHS R01 HL089617
6 · The paper itself

Abstract

Mesenchymal stem cell (MSC) transplantation after ischemia/reperfusion (I/R) injury reduces infarct size and improves cardiac function. We used mouse ventricular myocytes (VMs) in an in vitro model of I/R to determine the mechanism by which MSCs prevent reperfusion injury by paracrine signaling. Exposure of mouse VMs to an ischemic challenge depolarized their mitochondrial membrane potential (Ψmito), increased their diastolic Ca(2+), and significantly attenuated cell shortening. Reperfusion of VMs with Ctrl tyrode or MSC-conditioned tyrode (ConT) resulted in a transient increase of the Ca(2+) transient amplitudes in all cells. ConT-reperfused cells exhibited a decreased number early after depolarization (EADs) (ConT: 6.3% vs. Ctrl: 28.4%) and prolonged survival (ConT: 58% vs. Ctrl: 33%). Ψmito rapidly recovered in Ctrl as well as ConT-treated VMs on reperfusion; however, in Ctrl solution, an exaggerated hyperpolarization of Ψmito was determined that preceded the collapse of Ψmito. The ability of ConT to attenuate the hyperpolarization of Ψmito was suppressed on inhibition of the PI3K/Akt signaling pathway or IK,ATP. However, protection of Ψmito was best mimicked by the reactive oxygen species (ROS) scavenger mitoTEMPO. Analysis of ConT revealed a significant antioxidant capacity that was linked to the presence of extracellular superoxide dismutase (SOD3) in ConT. In conclusion, MSC ConT protects VMs from simulated I/R injury by its SOD3-mediated antioxidant capacity and by delaying the recovery of Ψmito through Akt-mediated opening of IK,ATP. These changes attenuate reperfusion-induced ROS production and prevent the opening of the permeability transition pore and arrhythmic Ca(2+) release.

Indexed as

Mesenchymal Stem Cell TransplantationAnimalsAntioxidantsBone Marrow CellsCalciumCells, CulturedCell SizeCell SurvivalIsotonic SolutionsMembrane Potential, MitochondrialMesenchymal Stem CellsMiceMice, Inbred C57BLMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacAntioxidantsCalciumIsotonic SolutionsMitoTEMPOOrganophosphorus CompoundsPiperidinesReactive Oxygen SpeciesSod3 protein, mouseSuperoxide DismutaseTyrode's solution

Identifiers

PMID23614555
PMCPMC3760058
OpenAlexW2102071079

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.