Evidence map›Paper›PMID 23593442›Full record

ArticlePloS one2013

Murine adipose tissue-derived stromal cell apoptosis and susceptibility to oxidative stress in vitro are regulated by genetic background.

Robert Pazdro, David E Harrison

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Heritability of in vitro phenotypes exhibited by murine adipose-derived stromal cells.Mammalian genome : official journal of the International Mammalian Genome Society · 2016
    Article
  2. Article
  3. Article
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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

2 authors at 1 institution in 1 country.

Robert PazdroThe Jackson Laboratory, Bar Harbor, Maine, United States of America.
David E Harrison
Jackson Laboratory · US

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI Anna Karolina Palucka · 1985 to 2026
$61.9M
Genetic Definition of Mechanisms by which Rapamycin Retards Mammalian AgingR01AG038560 · NIA · JACKSON LABORATORY · PI HARRISON, DAVID E · 2011 to 2015
$1.8M
Lifespan Extension Despite Greatly Elevated Insulin and Body FatR01AG032333 · NIA · JACKSON LABORATORY · PI HARRISON, DAVID E · 2010 to 2014
$1.8M
EXPERIMENTAL HEMATOLOGY-IMMUNOLOGYT32DK007449 · NIDDK · JACKSON LABORATORY · PI HARRISON, DAVID E · 1986 to 2012
$1.4M
Genetic Regulation of Glutathione Redox Balance in MiceF32GM101723 · NIGMS · JACKSON LABORATORY · PI PAZDRO, ROBERT · 2012 to 2013
$70k
NCI NIH HHS CA034196NCI NIH HHS P30 CA034196NIA NIH HHS AG032333NIA NIH HHS R01 AG032333NIA NIH HHS R01 AG038560NIDDK NIH HHS DK07449NIDDK NIH HHS T32 DK007449NIGMS NIH HHS F32 GM101723NIGMS NIH HHS GM101723
6 · The paper itself

Abstract

Adipose tissue-derived stromal cells (ADSCs) are of interest for regenerative medicine as they are isolated easily and can differentiate into multiple cell lineages. Studies of their in vitro proliferation, survival, and differentiation are common; however, genetic effects on these phenotypes remain unknown. To test if these phenotypes are genetically regulated, ADSCs were isolated from three genetically diverse inbred mouse strains--C57BL/6J (B6), BALB/cByJ (BALB), and DBA/2J (D2)--in which genetic regulation of hematopoietic stem function is well known. ADSCs from all three strains differentiated into osteogenic and chondrogenic lineages in vitro. ADSCs from BALB grew least well in vitro, probably due to apoptotic cell death after several days in culture. BALB ADSCs were also the most susceptible to the free radical inducers menadione and H2O2. ADSCs from the three possible F1 hybrids were employed to further define genetic regulation of ADSC phenotypes. D2, but not B6, alleles stimulated ADSC expansion in BALB cells. In contrast, B6, but not D2, alleles rescued BALB H2O2 resistance. We conclude that low oxidative stress resistance does not limit BALB ADSC growth in vitro, as these phenotypes are genetically regulated independently. In addition, ADSCs from these strains are an appropriate model system to investigate genetic regulation of ADSC apoptosis and stress resistance in future studies. Such investigations are essential to optimize cell expansion and differentiation and thus, potential for regenerative medicine.

Indexed as

Adipose TissueAnimalsApoptosisCell DifferentiationFemaleGene Expression RegulationMiceOxidative StressPhenotypeStromal Cells

Identifiers

PMID23593442
PMCPMC3617166
OpenAlexW2030435937

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.