Evidence map›Paper›PMID 29096706›Full record

ArticleStem cell research & therapy2017

Human iPSC-derived chondrocytes mimic juvenile chondrocyte function for the dual advantage of increased proliferation and resistance to IL-1β.

Jieun Lee, Piera Smeriglio, Constance R Chu, Nidhi Bhutani

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

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  16. Tissue Engineering for the Temporomandibular Joint.Advanced healthcare materials · 2019
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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

4 authors at 1 institution in 1 country.

Jieun LeeDepartment of Orthopaedic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Edwards Bldg., R164, Stanford, CA, 94305-5341, USA.
Piera SmeriglioDepartment of Orthopaedic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Edwards Bldg., R164, Stanford, CA, 94305-5341, USA.
Constance R ChuDepartment of Orthopaedic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Edwards Bldg., R164, Stanford, CA, 94305-5341, USA.
Nidhi BhutaniDepartment of Orthopaedic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Edwards Bldg., R164, Stanford, CA, 94305-5341, USA. nbhutani@stanford.edu.
Stanford University · US

Funding

Targeting DNA Demethylation Regulators in OsteoarthritisR01AR070865 · NIAMS · STANFORD UNIVERSITY · PI BHUTANI, NIDHI · 2016 to 2020
$1.7M
NIAMS NIH HHS R01 AR070865
6 · The paper itself

Abstract

backgroundInduced pluripotent stem cells (iPSC) provide an unlimited patient-specific cell source for regenerative medicine. Adult cells have had limited success in cartilage repair, but juvenile chondrocytes (from donors younger than 13 years of age) have been identified to generate superior cartilage. With this perspective, the aim of these studies was to compare the human iPSC-derived chondrocytes (hiChondrocytes) to adult and juvenile chondrocytes and identify common molecular factors that govern their function.

methodsPhenotypic and functional characteristics of hiChondrocytes were compared to juvenile and adult chondrocytes. Analyses of global gene expression profiling, independent gene expression, and loss-of-function studies were utilized to test molecular factors having a regulatory effect on hiChondrocytes and juvenile chondrocyte function.

resultsHere, we report that the iPSC-derived chondrocytes mimic juvenile chondrocytes in faster cell proliferation and resistance to IL-1β compared to adult chondrocytes. Whole genome transcriptome analyses revealed unique ECM factors and immune response pathways to be enriched in both juvenile and iPSC-derived chondrocytes as compared to adult chondrocytes. Loss-of-function studies demonstrated that CD24, a cell surface receptor enriched in both juvenile chondrocytes and hiChondrocytes, is a regulatory factor in both faster proliferation and resistance to proinflammatory cues in these chondrocyte populations.

conclusionsOur studies identify that hiChondrocytes mimic juvenile chondrocytes for the dual advantage of faster proliferation and a reduced response to the inflammatory cytokine IL-1β. While developmental immaturity of iPSC-derived cells can be a challenge for tissues like muscle and brain, our studies demonstrate that it is advantageous for a tissue like cartilage that has limited regenerative ability in adulthood.

Indexed as

AdultAge FactorsCartilage, ArticularCD24 AntigenCell DifferentiationCell ProliferationChondrocytesFemaleFetusGene Expression ProfilingGene Expression RegulationGene OntologyHumansInduced Pluripotent Stem CellsInfantInterleukin-1betaCD24 AntigenCD24 protein, humanIL1B protein, humanInterleukin-1betaCartilageCD24Human iPSC-derived chondrocytesInflammationJuvenile chondrocytes

Identifiers

PMID29096706
PMCPMC5667438
OpenAlexW2766986700

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.