Evidence map›Paper›PMID 25144720›Full record

ArticleCell death & disease2014

MicroRNA-302 induces proliferation and inhibits oxidant-induced cell death in human adipose tissue-derived mesenchymal stem cells.

J Y Kim, K K Shin, A L Lee, Y S Kim, H J Park, Y K Park, Y C Bae, J S Jung

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

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

31 citing papers in PubMed, 47 citations in OpenAlex.

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  18. Current Strategies to Enhance Adipose Stem Cell Function: An Update.International journal of molecular sciences · 2019
    Review
  19. Article
  20. Porous Se@SiOInternational journal of nanomedicine · 2019
    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

8 authors at 1 institution in 1 country.

J Y Kim1] Department of Physiology, School of Medicine, Pusan National University, Yangsan 626-870, Korea [2] Medical Research Center for Ischemic Tissue Engineering, Pusan National University, Yangsan 626-870, Korea [3] BK21 Medical Science Education Center, School of Medicine, Pusan National University, Yangsan 626-870, Korea.
K K Shin1] Department of Physiology, School of Medicine, Pusan National University, Yangsan 626-870, Korea [2] Medical Research Center for Ischemic Tissue Engineering, Pusan National University, Yangsan 626-870, Korea [3] BK21 Medical Science Education Center, School of Medicine, Pusan National University, Yangsan 626-870, Korea.
A L Lee1] Department of Physiology, School of Medicine, Pusan National University, Yangsan 626-870, Korea [2] Medical Research Center for Ischemic Tissue Engineering, Pusan National University, Yangsan 626-870, Korea [3] BK21 Medical Science Education Center, School of Medicine, Pusan National University, Yangsan 626-870, Korea.
Y S Kim1] Department of Physiology, School of Medicine, Pusan National University, Yangsan 626-870, Korea [2] Medical Research Center for Ischemic Tissue Engineering, Pusan National University, Yangsan 626-870, Korea [3] BK21 Medical Science Education Center, School of Medicine, Pusan National University, Yangsan 626-870, Korea.
H J Park1] Department of Physiology, School of Medicine, Pusan National University, Yangsan 626-870, Korea [2] Medical Research Center for Ischemic Tissue Engineering, Pusan National University, Yangsan 626-870, Korea [3] BK21 Medical Science Education Center, School of Medicine, Pusan National University, Yangsan 626-870, Korea.
Y K Park1] Department of Physiology, School of Medicine, Pusan National University, Yangsan 626-870, Korea [2] Medical Research Center for Ischemic Tissue Engineering, Pusan National University, Yangsan 626-870, Korea.
Y C BaeDepartment of Plastic Surgery, School of Medicine, Pusan National University, Pusan 602-739, Korea.
J S Jung1] Department of Physiology, School of Medicine, Pusan National University, Yangsan 626-870, Korea [2] Medical Research Center for Ischemic Tissue Engineering, Pusan National University, Yangsan 626-870, Korea [3] BK21 Medical Science Education Center, School of Medicine, Pusan National University, Yangsan 626-870, Korea [4] Medical Research Institute, Pusan National University, Pusan 602-739, Korea.
Pusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem cells (MSCs) are a heterogeneous population of cells that proliferate in vitro as plastic-adherent cells, have a fibroblast-like morphology, form colonies in vitro and can differentiate into bone, cartilage and fat cells. The abundance, ease and repeatable access to subcutaneous adipose tissue and the simple isolation procedures provide clear advantages for the use of human adipose tissue-derived mesenchymal stem cells (hASDCs) in clinical applications. We screened microRNAs (miRNAs) that affected the proliferation and survival of hADSCs. Transfection of miR-302d mimic increased cell proliferation and protected cells from oxidant-induced cell death in hADSCs, which was supported by flow-cytometric analysis. miR-302d did not affect the expression of Bcl-2 family members or anti-oxidant molecules. The Nrf2-Keap1 system, which is one of the major mechanisms for the cellular defense against oxidative stress, was not altered by transfection of miR-302d mimic. To identify the target of the miR-302d actions on proliferation and survival of hADSCs, a microarray analysis was performed using miR-302d-overexpressing hADSCs. Real-time PCR analysis showed that transfection of miR-302d mimic inhibited the CDKN1A and CCL5 expression. Downregulation of CDKN1A with a specific siRNA mimicked the effect of miR-302d on hADSCs proliferation, but did not affect miR-302d-induced cell survival. Downregulation of CCL5 protected oxidant-induced cell death as miR-302d, inhibited oxidant-induced reactive oxygen species (ROS) generation and the addition of recombinant CCL5 inhibited the protective action of miR-302d on oxidant-induced cell death. This study indicates that miR-302 controls proliferation and cell survival of hADSCs through different targets and that this miRNA can be used to enhance the therapeutic efficacy of hADSCs transplantation in vivo.

Indexed as

Adipose TissueApoptosisBase SequenceCell DifferentiationCell ProliferationCells, CulturedChemokine CCL5CobaltCyclin-Dependent Kinase Inhibitor p21Down-RegulationG1 Phase Cell Cycle CheckpointsHeme Oxygenase-1HumansIntracellular Signaling Peptides and ProteinsKelch-Like ECH-Associated Protein 1Mesenchymal Stem CellsChemokine CCL5Cobaltcobaltous chlorideCyclin-Dependent Kinase Inhibitor p21Heme Oxygenase-1HMOX1 protein, humanIntracellular Signaling Peptides and ProteinsKEAP1 protein, humanKelch-Like ECH-Associated Protein 1linsidomineMicroRNAsMolsidomineNFE2L2 protein, humanNF-E2-Related Factor 2Oligonucleotides, AntisenseProto-Oncogene Proteins c-bcl-2Reactive Oxygen Species

Identifiers

PMID25144720
PMCPMC4454318
OpenAlexW2150542193

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.