Evidence map›Paper›PMID 21899882›Full record

ArticleBiomaterials2011

Actin and ERK1/2-CEBPβ signaling mediates phagocytosis-induced innate immune response of osteoprogenitor cells.

Heon Goo Lee, Hiroshi Minematsu, Kyung Ok Kim, Ayse B Celil Aydemir, Mike J Shin, Saqib A Nizami, Kook Jin Chung, Anny C Hsu, Christopher R Jacobs, Francis Youngin Lee

Abstract read
In one paragraph

Article in Biomaterials, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. The Effects of Biomaterial Implant Wear Debris on Osteoblasts.Frontiers in cell and developmental biology · 2020
    Review
  10. Review
  11. Article
  12. Remifentanil upregulates hepatic IL-18 binding protein (IL-18BP) expression through transcriptional control.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
  13. Article
  14. Article
  15. Mesenchymal stem cells in the aseptic loosening of total joint replacements.Journal of biomedical materials research. Part A · 2017
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

10 authors at 2 institutions in 2 countries.

Heon Goo LeeDepartment of Orthopaedic Surgery, Columbia University College of Physicians and Surgeons, NY 10032, USA.
Hiroshi Minematsu
Kyung Ok Kim
Ayse B Celil Aydemir
Mike J Shin
Saqib A Nizami
Kook Jin Chung
Anny C Hsu
Christopher R Jacobs
Francis Youngin Lee
Columbia University · USHallym University Kangnam Sacred Heart Hospital · KR

Funding

ERK Signaling in Inflammatory Bone LossR01AR056246 · NIAMS · YALE UNIVERSITY · PI LEE, FRANCIS YOUNG-IN · 2009 to 2018
$3.5M
Mechanobiological Mechanism for Inflammatory Bone LossR01EB006834 · NIBIB · YALE UNIVERSITY · PI LEE, FRANCIS YOUNG-IN · 2007 to 2015
$2.6M
NIAMS NIH HHS R01 AR056246NIAMS NIH HHS R01AR056246NIBIB NIH HHS R01 EB006834NIBIB NIH HHS R01EB006834
6 · The paper itself

Abstract

Wear particles at the host bone-implant interface are a major challenge for successful bone implant arthoplasties. Current understanding of aseptic loosening consists of macrophage-mediated inflammatory responses and increasing osteoclastogenesis, which lead to an imbalance between bone formation and resorption. Despite its significant role in bone regeneration and implant osteointegration, the osteoprogenitor response to wear particles has been examined recent years. More specifically, the intracellular mechanism of osteoprogenitor mediated inflammation has not been fully elucidated. In this study, we examined the role of osteoprogenitors and the cellular mechanism by which metal wear particles elicit an inflammatory cascade. Through both in vivo and in vitro experiments, we have demonstrated that osteoprogenitor cells are capable of initiating inflammatory responses by phagocytosing wear particles, which lead to subsequent accumulation of macrophages and osteoclastogenesis, and the ERK_CEBP/β intracellular signaling is a key inflammatory pathway that links phagocytosis of wear particles to inflammatory gene expression in osteoprogenitors. AZD6244 treatment, a potent inhibitor of the ERK pathway, attenuated particle mediated inflammatory osteolysis both in vivo and in vitro. This study advances our understanding of the mechanisms of osteoprogenitor-mediated inflammation, and provides further evidence that the ERK_CEBP/β pathway may be a suitable therapeutic target in the treatment of inflammatory osteolysis.

Indexed as

ActinsAdhesivenessAnimalsBenzimidazolesBone and BonesCCAAT-Enhancer-Binding Protein-betaCyclooxygenase 2Cytochalasin DExtracellular Signal-Regulated MAP KinasesGene Expression RegulationHumansImmunity, InnateInflammationInterleukin-6MAP Kinase Signaling SystemMiceActinsAZD 6244BenzimidazolesCCAAT-Enhancer-Binding Protein-betaCyclooxygenase 2Cytochalasin DExtracellular Signal-Regulated MAP KinasesInterleukin-6Protein Kinase InhibitorsPtgs2 protein, mouseTitanium

Identifiers

PMID21899882
PMCPMC3193180
OpenAlexW2071689310

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.