Evidence map›Paper›PMID 28646230›Full record

ArticleScientific reports2017

IL-1β increases asporin expression via the NF-κB p65 pathway in nucleus pulposus cells during intervertebral disc degeneration.

Shengjie Wang, Chao Liu, Zhongyi Sun, Peng Yan, He Liang, Kai Huang, Changwei Li, Jiwei Tian

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. ASPORIN: A root of the matter in tumors and their host environment.Biochimica et biophysica acta. Reviews on cancer · 2024
    Review
  5. Article
  6. Review
  7. Observational
  8. Review
  9. Article
  10. HIF-1Oxidative medicine and cellular longevity · 2021
    Article
  11. Article
  12. Apigenin Mitigates Intervertebral Disc Degeneration through the Amelioration of Tumor Necrosis Factor α (TNF-α) Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  13. Article
  14. Article
  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

8 authors at 4 institutions in 1 country.

Shengjie WangDepartment of Orthopedics, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, 100, Haining Road, Shanghai, 200080, People's Republic of China.
Chao LiuDepartment of Orthopedics, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, 100, Haining Road, Shanghai, 200080, People's Republic of China.
Zhongyi SunDepartment of Orthopedics, Songjiang District Central Hospital of Shanghai, 746, middle-Zhongshan Road, Shanghai, 201600, People's Republic of China.
Peng YanDepartment of Orthopedics, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, 100, Haining Road, Shanghai, 200080, People's Republic of China.
He LiangDepartment of Orthopedics, Songjiang District Central Hospital of Shanghai, 746, middle-Zhongshan Road, Shanghai, 201600, People's Republic of China.
Kai HuangDepartment of Orthopedics, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, 100, Haining Road, Shanghai, 200080, People's Republic of China.
Changwei LiShanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases with Integrated Chinese-Western Medicine, Shanghai Institute of Traumatology and Orthopedics, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai, 200025, People's Republic of China. changwei393331@163.com.
Jiwei TianDepartment of Orthopedics, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, 100, Haining Road, Shanghai, 200080, People's Republic of China. tjw609@163.com.
Shanghai Jiao Tong University · CNShanghai First People's Hospital · CNSongjiang District Central Hospital · CNRuijin Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disc degeneration (DD) is a multifaceted chronic process that alters the structure and function of intervertebral discs. The pathophysiology of degeneration is not completely understood, but the consensus is that changes in genes encoding extracellular matrix (ECM) proteins in the disc are the leading factors contributing to DD. Asporin is an ECM protein that has been shown to be increased in degenerated intervertebral discs, but little is known about how asporin is regulated during DD. In exploring the intricate mechanism, we confirmed that asporin was abundantly increased in patients' degenerated nucleus pulposus. Consistently, the increased asporin expression with degeneration was also proved by rabbit intervertebral disc degeneration (IDD) model. Mechanistically, IL-1β upregulated asporin expression by activating the p65 pathway in human nucleus pulposus cells. Furthermore, p65 mediated asporin expression by binding to -41/-31 bp on asporin promoter. Functionally, asporin was the intermediator of IL-1β-inhibited aggrecan and collagen Π expression and played a negative role in TGF-β-induced aggrecan and collagen Π formation in human nucleus pulposus cells. Therefore, identifying asporin as a negative regulator of aggrecan and collagen Π and elucidating its induction mechanisms in human nucleus pulposus cells provides new insight for asporin induction during IDD.

Indexed as

Signal TransductionAdolescentAdultAnimalsBinding SitesCollagenDisease Models, AnimalExtracellular Matrix ProteinsFemaleGene Expression RegulationGene Knockdown TechniquesGenes, ReporterHumansInterleukin-1betaIntervertebral Disc DegenerationMagnetic Resonance ImagingASPN protein, humanCollagenExtracellular Matrix ProteinsInterleukin-1betaTranscription Factor RelA

Identifiers

PMID28646230
PMCPMC5482889
OpenAlexW2661488461

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Registered trials

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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.