Evidence map›Paper›PMID 24131310›Full record

ArticleTissue engineering. Part A2014

Lysophosphatidic acid protects human mesenchymal stromal cells from differentiation-dependent vulnerability to apoptosis.

Bernard Y K Binder, Damian C Genetos, J Kent Leach

Abstract read
In one paragraph

Article in Tissue engineering. Part A, 2014. 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
3.1field-weighted citation impact, top 8% 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, 36 citations in OpenAlex.

  1. Article
  2. Article
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  4. Co-stimulation of LPARStem cell research & therapy · 2018
    Article
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  15. Hydrogel biophysical properties instruct coculture-mediated osteogenic potential.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  16. Review
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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

3 authors at 1 institution in 1 country.

Bernard Y K Binder1 Department of Biomedical Engineering, University of California , Davis, Davis, California.
Damian C Genetos
J Kent Leach
University of California, Davis · US

Funding

Engineering Approaches to Molecular Imaging TrainingT32EB003827 · NIBIB · UNIVERSITY OF CALIFORNIA DAVIS · PI FERRARA, KATHERINE W · 2004 to 2013
$1.6M
Phospholipids for enhancing cell-based neovascularizationR21AG036963 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LEACH, J. KENT · 2010 to 2011
$339k
Regulation of sclerostin expression by hypoxia: A proposed mechanism to explain hR03AR057547 · NIAMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GENETOS, DAMIAN C · 2010 to 2012
$224k
NIAMS NIH HHS R03 AR057547NIA NIH HHS 1R21AG036963NIA NIH HHS R21 AG036963NIBIB NIH HHS T32EB003827
6 · The paper itself

Abstract

The survival of transplanted cells and their resulting efficacy in cell-based therapies is markedly impaired due to serum deprivation and hypoxia (SD/H) resulting from poor vascularization within tissue defects. Lysophosphatidic acid (LPA) is a platelet-derived growth factor with pleiotropic effects on many cell types. Mesenchymal stromal cells (MSC) exhibit unique secretory and stimulatory characteristics depending on their differentiation state. In light of the potential of MSC in cell-based therapies, we examined the ability of LPA to abrogate SD/H-induced apoptosis in human MSC at increasing stages of osteogenic differentiation in vitro and assessed MSC survival in vivo. Undifferentiated MSC were rescued from SD/H-induced apoptosis by treatment with both 25 and 100 μM LPA. However, MSC conditioned with osteogenic supplements responded to 25 μM LPA, and cells conditioned with dexamethasone-containing osteogenic media required 100 μM LPA. This rescue was mediated through LPA1 in all cases. The addition of 25 μM LPA enhanced vascular endothelial growth factor (VEGF) secretion by MSC in all conditions, but VEGF availability was not responsible for protection against apoptosis. We also showed that codelivery of 25 μM LPA with MSC in alginate hydrogels significantly improved the persistence of undifferentiated MSC in vivo over 4 weeks as measured by bioluminescence imaging. Osteogenic differentiation alone was protective of SD/H-induced apoptosis in vitro, and the synergistic delivery of LPA did not enhance persistence of osteogenically induced MSC in vivo. These data demonstrate that the capacity of LPA to inhibit SD/H-induced apoptosis in MSC is dependent on both the differentiation state and dosage. This information will be valuable for optimizing osteogenic conditioning regimens for MSC before in vivo implementation.

Indexed as

AnimalsApoptosisCell DifferentiationCell HypoxiaCell ProliferationCell SurvivalCulture Media, Serum-FreeCytoprotectionHumansLysophospholipidsMesenchymal Stem CellsMiceOsteogenesisReceptors, Lysophosphatidic AcidVascular Endothelial Growth Factor ACulture Media, Serum-Freelysophosphatidic acidLysophospholipidsReceptors, Lysophosphatidic AcidVascular Endothelial Growth Factor A

Identifiers

PMID24131310
PMCPMC3993074
OpenAlexW1184394672

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.