Evidence map›Paper›PMID 29228588›Full record

ArticleOncotarget2017

Interleukin-17A-promoted MSC2 polarization related with new bone formation of ankylosing spondylitis.

Tao He, Yan Huang, Chen Zhang, Denghui Liu, Chao Cheng, Weidong Xu, Xiaoling Zhang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 28% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Uncovering the Underworld of Axial Spondyloarthritis.International journal of molecular sciences · 2023
    Review
  8. Review
  9. Review
  10. Article
  11. 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

7 authors at 4 institutions in 1 country.

Tao HeDepartment of Joint Surgery and Sports Medicine, Changhai Hospital Affiliated to the Second Military Medical University, Shanghai, People's Republic of China.
Yan HuangThe Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, People's Republic of China.
Chen ZhangDepartment of Joint Surgery and Sports Medicine, Changhai Hospital Affiliated to the Second Military Medical University, Shanghai, People's Republic of China.
Denghui LiuDepartment of Joint Surgery and Sports Medicine, Changhai Hospital Affiliated to the Second Military Medical University, Shanghai, People's Republic of China.
Chao ChengDepartment of Nuclear Medicine, Changhai Hospital Affiliated to the Second Military Medical University, Shanghai, People's Republic of China.
Weidong XuDepartment of Joint Surgery and Sports Medicine, Changhai Hospital Affiliated to the Second Military Medical University, Shanghai, People's Republic of China.
Xiaoling ZhangThe Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, People's Republic of China.
Changhai Hospital · CNChinese Academy of Sciences · CNSecond Military Medical University · CNXinHua Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It's still unknown how over-hyperplasia of tissue such like new bone formation (NBF) developed in ankylosing spondylitis (AS). We found low level of IL-17A promoted TLR4+MSC1 polarization with suppressed osteogenic differentiation through JAK2/STAT3 pathway, while high level of IL-17A promoted TLR3+MSC2 polarization with enhanced osteogenic differentiation through WNT10b/RUNX2 pathway. Furthermore, both proteoglycan-induced spondylitis (PGISp) mouse model and AS patients without NBF showed MSC1 polarization, up-regulated JAK2/STAT3 pathway and high level of IL-17A (peripherally, but not locally), but those with NBF showed MSC2 polarization, up-regulated WNT10b/RUNX2 pathway and high expression of IL-17A at local site. Results showed NBF of AS was induced by MSC2 polarization that was promoted by high level of IL-17A, and may be treated by suppressing local MSC2 polarization.

Indexed as

ankylosing spondylitisinterleukin-17mesenchymal stem cellsnew bone formationpolarization

Identifiers

PMID29228588
PMCPMC5722540
OpenAlexW2755484791

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.