Evidence map›Paper›PMID 31753397›Full record

ArticleMaterials science & engineering. C, Materials for biological applications2020

Synovium stem cell-derived matrix enhances anti-inflammatory properties of rabbit articular chondrocytes via the SIRT1 pathway.

Jinku Yan, Xi Chen, Chengbo Pu, Yilang Zhao, Xiaozhen Liu, Tao Liu, Guoqing Pan, Jun Lin, Ming Pei, Huilin Yang and 1 more

Erratum issuedOpen access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Materials science & engineering. C, Materials for biological applications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 2 countries.

Jinku YanDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China; Orthopaedic Institute, Medical College, Soochow University, Suzhou, 215007, China; The Experimental Center, Cancer Hospital of the University of Chinese Academy of Sciences, Hangzhou, 310022, China.
Xi ChenDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China; Orthopaedic Institute, Medical College, Soochow University, Suzhou, 215007, China.
Chengbo PuDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China; Orthopaedic Institute, Medical College, Soochow University, Suzhou, 215007, China.
Yilang ZhaoDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China; Orthopaedic Institute, Medical College, Soochow University, Suzhou, 215007, China.
Xiaozhen LiuThe Experimental Center, Cancer Hospital of the University of Chinese Academy of Sciences, Hangzhou, 310022, China.
Tao LiuDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China. Electronic address: liutao8250@suda.edu.cn.
Guoqing PanInstitute for Advanced Materials, School of Materials Science and Engineering, Jiangsu University, Zhenjiang, 212013, China.
Jun LinDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Ming PeiStem Cell and Tissue Engineering Laboratory, Department of Orthopaedics and Division of Exercise Physiology, West Virginia University, Morgantown, WV, 26506, USA.
Huilin YangDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China; Orthopaedic Institute, Medical College, Soochow University, Suzhou, 215007, China.
Fan HeDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China; Orthopaedic Institute, Medical College, Soochow University, Suzhou, 215007, China. Electronic address: fanhe@suda.edu.cn.
Soochow University · CNFirst Affiliated Hospital of Soochow University · CNUniversity of Chinese Academy of Sciences · CNJiangsu University · CNWest Virginia University · US

Funding

Decellularized Matrix and Cartilage RegenerationR01AR067747 · NIAMS · WEST VIRGINIA UNIVERSITY · PI PEI, MING · 2016 to 2020
$1.7M
NIAMS NIH HHS R01 AR067747
6 · The paper itself

Abstract

Autologous chondrocyte implantation (ACI) is a promising approach to repair cartilage defects; however, the cartilage trauma-induced inflammatory environment compromises its clinical outcomes. Cell-derived decellularized extracellular matrix (DECM) has been used as a culture substrate for mesenchymal stem cells (MSCs) to improve the cell proliferation and lineage-specific differentiation. In this study, DECM deposited by synovium-derived MSCs was used as an in vitro expansion system for rabbit articular chondrocytes and the response of DECM-expanded chondrocytes to pro-inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) was evaluated. Compared with those grown on tissue culture polystyrene (TCPS), the proliferation rate was significantly improved in DECM-expanded chondrocytes. TCPS- and DECM-expanded chondrocytes were isolated and induced to redifferentiation in a high-density pellet culture. DECM-expanded chondrocytes exerted a stronger resistance to 1 ng/mL of IL-1β than TCPS-expanded cells, but the production of cartilage matrix in both groups was inhibited by 5 ng/mL of IL-1β. When exposed to 1 or 5 ng/mL of TNF-α, DECM-expanded chondrocytes showed higher levels of cartilage matrix synthesis than TCPS-expanded cells. In addition, the gene expression of IL-1β- or TNF-α-induced matrix degrading enzymes (MMP3, MMP9, MMP13, and ADAMTS5) was significantly lower in DECM-expanded chondrocytes than TCPS-expanded cells. Furthermore, we found that SIRT1 inhibition by nicotinamide completely counteracted the protective effect of DECM on chondrocytes in the presence of IL-1β or TNF-α, indicating that the SIRT1 signaling pathway was involved in the DECM-mediated enhancement of anti-inflammatory properties of chondrocytes. Taken together, this work suggests that stem cell-derived DECM is a superior culture substrate for in vitro chondrocyte expansion by improving proliferation and enhancing the anti-inflammatory properties of chondrocytes. DECM-expanded chondrocytes with enhanced anti-inflammatory properties hold great potential in clinically ACI-based cartilage repair.

Indexed as

AggrecansAnimalsCartilage, ArticularCell Culture TechniquesCell ProliferationChondrocytesCulture Media, ConditionedDown-RegulationExtracellular MatrixInterleukin-1betaMesenchymal Stem CellsRabbitsSignal TransductionSirtuin 1SOX9 Transcription FactorSynovial MembraneAggrecansCulture Media, ConditionedInterleukin-1betaSirtuin 1SOX9 Transcription FactorTumor Necrosis Factor-alphaChondrocytesDecellularizedExtracellular matrixIL-1βSIRT1TNF-α

Identifiers

PMID31753397
PMCPMC9805357
OpenAlexW2980133414

What OpenQuestion holds

Textmetadata
LicenceTDM
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.