Evidence map›Paper›PMID 26066979›Full record

ArticleScientific reports2015

COX2 is involved in hypoxia-induced TNF-α expression in osteoblast.

Yonggang Xing, Renxian Wang, Dafu Chen, Jianping Mao, Rui Shi, Zhihong Wu, Jun Kang, Wei Tian, Chi Zhang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
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  9. Article
  10. Review
  11. Hypoxia Induces MacrophageFrontiers in immunology · 2019
    Article
  12. Article
  13. Article
  14. Review
  15. Article
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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

9 authors at 4 institutions in 2 countries.

Yonggang XingDepartment of Spine, Beijing JiShuiTan Hospital, Beijing, 100035, China.
Renxian WangBeijing Laboratory of Biomedical Materials, Laboratory of Bone Tissue Engineering, Beijing Research Institute of Traumatology and Orthopaedics, Beijing JiShuiTan Hospital, Beijing 100035, China.
Dafu ChenBeijing Laboratory of Biomedical Materials, Laboratory of Bone Tissue Engineering, Beijing Research Institute of Traumatology and Orthopaedics, Beijing JiShuiTan Hospital, Beijing 100035, China.
Jianping MaoDepartment of Spine, Beijing JiShuiTan Hospital, Beijing, 100035, China.
Rui ShiBeijing Laboratory of Biomedical Materials, Laboratory of Bone Tissue Engineering, Beijing Research Institute of Traumatology and Orthopaedics, Beijing JiShuiTan Hospital, Beijing 100035, China.
Zhihong WuDepartment of Orthopedic Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, 100730, China.
Jun KangDepartment of Periodontology, School and Hospital of Stomatology, Peking University, Beijing, 100081, China.
Wei TianDepartment of Spine, Beijing JiShuiTan Hospital, Beijing, 100035, China.
Chi ZhangBone Research Laboratory, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Peking University · CNBeijing Jishuitan Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNThe University of Texas Southwestern Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone regeneration involves a series of events in a coordinated manner, including recruitment of mesenchymal stem cells, induction of immune response, inflammatory activity and vascular ingrowth. The microenvironment of bone regeneration is hypoxic. Low oxygen tension (hypoxia) promotes the upregulation of several signaling molecules. The primary mediating factor is the hypoxia-inducible factor-1 (HIF-1). Hypoxia stimulates the expression of a variety of cytokines from inflammatory cells, fibroblasts, endothelial cells, and osteoblasts. TNF-α is a key proinflammatory cytokine. The molecular events involved in osteoblast dysfunction under hypoxia are not fully understood. This study determined the effects of hypoxia on TNF-α in osteoblasts, and molecular mechanisms were explored. We observed that hypoxia induced TNF-α expression in a time-dependent manner in osteoblasts. Experiments using a potent HIF-1α activator DFO demonstrated that hypoxia-induced TNF-α was mediated by HIF-1-α. In addition, this study showed that hypoxia activated cyclooxygenase-2 (COX2) expression along with TNF-α. Inhibition experiments using COX2 inhibitor N398 indicated that COX2 was involved in hypoxia-mediated TNF-α expression, and this observation was further confirmed by Small interfering RNA against COX2. On the other hand, TNF-α didn't lead to the activation of COX2 expression. We conclude that COX2 is involved in hypoxia-induced TNF-α expression in osteoblast.

Indexed as

Gene Expression RegulationAnimalsCell HypoxiaCell LineCyclooxygenase 2Cyclooxygenase 2 InhibitorsMiceOsteoblastsTumor Necrosis Factor-alphaCyclooxygenase 2Cyclooxygenase 2 InhibitorsPtgs2 protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID26066979
PMCPMC4464352
OpenAlexW2271921044

What OpenQuestion holds

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LicenceCC BY
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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.