Evidence map›Paper›PMID 22435530›Full record

ArticleJournal of cellular and molecular medicine2012

Mesenchymal stem cells conditioned with glucose depletion augments their ability to repair-infarcted myocardium.

Mahmood S Choudhery, Mohsin Khan, Ruhma Mahmood, Sadia Mohsin, Shoaib Akhtar, Fatima Ali, Shaheen N Khan, Sheikh Riazuddin

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

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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

8 authors.

Mahmood S ChoudheryNational Center of Excellence in Molecular Biology, University of the Punjab, Lahore, Pakistan.
Mohsin Khan
Ruhma Mahmood
Sadia Mohsin
Shoaib Akhtar
Fatima Ali
Shaheen N Khan
Sheikh Riazuddin

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem cells (MSCs) are an attractive candidate for autologous cell therapy, but their ability to repair damaged myocardium is severely compromised with advanced age. Development of viable autologous cell therapy for treatment of heart failure in the elderly requires the need to address MSC ageing. In this study, MSCs from young (2 months) and aged (24 months) C57BL/6 mice were characterized for gene expression of IGF-1, FGF-2, VEGF, SIRT-1, AKT, p16(INK4a) , p21 and p53 along with measurements of population doubling (PD), superoxide dismutase (SOD) activity and apoptosis. Aged MSCs displayed senescent features compared with cells isolated from young animals and therefore were pre-conditioned with glucose depletion to enhance age affected function. Pre-conditioning of aged MSCs led to an increase in expression of IGF-1, AKT and SIRT-1 concomitant with enhanced viability, proliferation and delayed senescence. To determine the myocardial repair capability of pre-conditioned aged MSCs, myocardial infarction (MI) was induced in 24 months old C57BL/6 wild type mice and GFP expressing untreated and pre-conditioned aged MSCs were transplanted. Hearts transplanted with pre-conditioned aged MSCs showed increased expression of paracrine factors, such as IGF-1, FGF-2, VEGF and SDF-1α. This was associated with significantly improved cardiac performance as measured by dp/dt(max), dp/dt(min), LVEDP and LVDP, declined left ventricle (LV) fibrosis and apoptosis as measured by Masson's Trichrome and TUNEL assays, respectively, after 30 days of transplantation. In conclusion, pre-conditioning of aged MSCs with glucose depletion can enhance proliferation, delay senescence and restore the ability of aged cells to repair senescent infarcted myocardium.

Indexed as

Mesenchymal Stem Cell TransplantationAnimalsApoptosisCell ProliferationCells, CulturedCell SurvivalCellular SenescenceFibroblast Growth Factor 2FibrosisGene Expression ProfilingGene Expression RegulationGlucoseInsulin-Like Growth Factor IKineticsMesenchymal Stem CellsMiceFibroblast Growth Factor 2Glucoseinsulin-like growth factor-1, mouseInsulin-Like Growth Factor IProto-Oncogene Proteins c-aktSirt1 protein, mouseSirtuin 1Superoxide DismutaseVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID22435530
PMCPMC3823444

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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.