Evidence map›Paper›PMID 29526830›Full record

ArticleActa biomaterialia2018

Inhibition of osteoclastogenesis by stem cell-derived extracellular matrix through modulation of intracellular reactive oxygen species.

Mao Li, Xi Chen, Jinku Yan, Long Zhou, Yifan Wang, Fan He, Jun Lin, Caihong Zhu, Guoqing Pan, Jia Yu and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta biomaterialia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.3field-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

29 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. OptimizingPeerJ · 2026
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  8. Extracellular derivatives for bone metabolism.Journal of advanced research · 2024
    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

13 authors at 3 institutions in 2 countries.

Mao LiDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou 215006, China; Orthopaedic Institute, Medical College, Soochow University, Suzhou 215007, China.
Xi ChenDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou 215006, China; Orthopaedic Institute, Medical College, Soochow University, Suzhou 215007, China; School of Biology and Basic Medical Sciences, Medical College, Soochow University, Suzhou 215123, China.
Jinku YanDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou 215006, China; Orthopaedic Institute, Medical College, Soochow University, Suzhou 215007, China.
Long ZhouDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou 215006, China; Orthopaedic Institute, Medical College, Soochow University, Suzhou 215007, China.
Yifan WangDepartment 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.
Jun LinDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Caihong ZhuDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou 215006, China; Orthopaedic Institute, Medical College, Soochow University, Suzhou 215007, China.
Guoqing PanDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou 215006, China; Orthopaedic Institute, Medical College, Soochow University, Suzhou 215007, China.
Jia YuDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou 215006, China; Orthopaedic Institute, Medical College, Soochow University, Suzhou 215007, 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.
Tao LiuDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. Electronic address: liutao8250@suda.edu.cn.
Soochow University · CNFirst Affiliated Hospital of Soochow 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

Decellularized extracellular matrix (ECM) derived from stem cells has been shown as a promising biomaterial for bone regeneration because of the promotion effect on osteogenesis in mesenchymal stem cells (MSCs). However, bone regeneration is also influenced by bone resorption and little is known about the effect of cell-derived ECM on osteoclast differentiation. In this study, ECM was deposited by MSCs and, after decellularization, the effect of ECM on osteoclastogenesis of bone marrow monocytes (BMMs) was investigated in comparison to standard tissue culture polystyrene. Our results showed that cell-derived ECM improved BMM proliferation but potently inhibited osteoclast differentiation, evidenced by down-regulation of multinucleated tartrate-resistant acid phosphatase (TRAP)-positive cells, areas of actin rings, and osteoclast-specific gene expression. ECM-mediated attenuation of intracellular reactive oxygen species (ROS) was suggested to play a rival role in the inhibition of osteoclastogenesis, because exogenous hydrogen peroxide supplementation partially rescued the ECM-inhibited osteoclastogenesis. Furthermore, rather than collagen type I, fibronectin in the ECM contributed to ECM-mediated anti-osteoclastogenesis. In conclusion, stem cell-derived decellularized ECM significantly suppressed osteoclastogenesis via the attenuation of intracellular ROS. The anti-osteoclastogenic property of cell-derived ECM may benefit its clinical use for modulating bone remodeling and promoting bone tissue engineering. STATEMENT OF SIGNIFICANCE: Decellularized extracellular matrix (ECM) derived from stem cells has been shown as a promising biomaterial for bone regeneration; however, bone remodeling is influenced by bone resorption and little is known about the effect of cell-derived ECM on osteoclast differentiation. Cell-derived ECM improved BMM proliferation but potently inhibited osteoclast differentiation. ECM-mediated attenuation of intracellular reactive oxygen species was suggested to play a rival role in osteoclastogenesis. Fibronectin in cell-derived ECM also contributed to ECM-mediated anti-osteoclastogenesis. The anti-osteoclastogenic property of cell-derived ECM may benefit clinically for modulating bone remodeling and promoting bone tissue engineering.

Indexed as

AnimalsBone Marrow CellsExtracellular MatrixMaleMesenchymal Stem CellsMiceOsteoclastsReactive Oxygen SpeciesReactive Oxygen SpeciesBone marrow monocytesExtracellular matrixNF-κBOsteoclastsReactive oxygen species

Identifiers

PMID29526830
PMCPMC5899936
OpenAlexW2794329260

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.