Evidence map›Paper›PMID 27627724›Full record

ArticleOrthopaedic surgery2016

Intermittent Cyclic Mechanical Tension Promotes Degeneration of Endplate Cartilage via the Nuclear Factor-κB Signaling Pathway: an in Vivo Study.

Liang Xiao, Hong-Guang Xu, Hong Wang, Ping Liu, Chen Liu, Xiang Shen, Tao Zhang, Yong-Ming Xu

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Article in Orthopaedic surgery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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  8. Article
  9. [Expression and significance of hypoxia-inducible factor 1α in endplate chondrocytes of rats].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2017
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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 1 institution in 1 country.

Liang XiaoDepartment of Orthopaedic Surgery, Yijishan Hospital, Wannan Medical College, Wuhu, China.
Hong-Guang XuDepartment of Orthopaedic Surgery, Yijishan Hospital, Wannan Medical College, Wuhu, China. xlllan2012@126.com.
Hong WangDepartment of Orthopaedic Surgery, Yijishan Hospital, Wannan Medical College, Wuhu, China.
Ping LiuDepartment of Orthopaedic Surgery, Yijishan Hospital, Wannan Medical College, Wuhu, China.
Chen LiuDepartment of Orthopaedic Surgery, Yijishan Hospital, Wannan Medical College, Wuhu, China.
Xiang ShenDepartment of Orthopaedic Surgery, Yijishan Hospital, Wannan Medical College, Wuhu, China.
Tao ZhangDepartment of Orthopaedic Surgery, Yijishan Hospital, Wannan Medical College, Wuhu, China.
Yong-Ming XuDepartment of Orthopaedic Surgery, Yijishan Hospital, Wannan Medical College, Wuhu, China.
Wannan Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo establish a rabbit model for investigating the effects of intermittent cyclic mechanical tension (ICMT) on promoting degeneration of endplate cartilage.

methodsForty New Zealand white rabbits were subjected to surgery and randomly divided into three equal groups as follows: control group (no treatment, n = 10), sham group (animals underwent a sham operation but were not subjected to mechanical tensile strain, n = 15) and loaded group (discs were subjected to 1.5 MPa external tensile loading by using an external loading device during the animals' daily activity, n = 15). Mechanical tensile strain was applied for 8 h/d. The animals were examined radiologically after 8 weeks treatment and then killed for removal of endplate cartilage tissue samples from their spines. Histological staining was performed to examine the morphology of endplate cartilage tissue. Multiple strategies were employed to examine degeneration of endplate cartilage and nuclear factor (NF)-κB signaling pathway activation.

resultsAfter ICMT loading for 56 days, radiology revealed ossification, hyperosteogeny and stenosis in the intervertebral spaces. Examination of hematoxylin and eosin staining of sections of endplate cartilage showed significant damage as the load duration increased in the ICMT loading group. Expression of aggrecan (ACAN), type II collagen (COL-2A), SRY-related high mobility group-box gene 9 (SOX9) was down-regulated (FACAN = 21.515, P < 0.01; FCOL-2A = 6.670, P = 0.05; FSOX9 = 7.888, P < 0.05), whereas that of matrix metallopeptidase 13 (MMP13) was up-regulated (FMMP13 = 14.120, P < 0.01) after ICMT. Western blot and immunofluorescence revealed that expression of protein was consistent with gene expression results. Additionally, ICMT loading can lead to NF-κB signaling pathway activation as well as degeneration of endplate cartilage.

conclusionThese experiments indicate that ICMT contributes to the activation of NF-κB signaling pathway in vivo and that the NF-κB signaling pathway further up-regulates MMP13, leading to degeneration of endplate cartilage.

Indexed as

Signal TransductionAnimalsBiomarkersBiomechanical PhenomenaBlotting, WesternImmunohistochemistryIntervertebral DiscMaleNF-kappa BRabbitsRadiographyRandom AllocationStress, PhysiologicalUp-RegulationWeight-BearingBiomarkersNF-kappa BEndplate cartilage degenerationIntermittent cyclic mechanical tensionIn vivoNF-κF signaling pathway

Identifiers

PMID27627724
PMCPMC6584380
OpenAlexW2528758537

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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.