Evidence map›Paper›PMID 24085277›Full record

ArticleEuropean journal of histochemistry : EJH2013

Continuous cyclic mechanical tension increases ank expression in endplate chondrocytes through the TGF-β1 and p38 pathway.

H Xu, X Zhang, H Wang, Y Zhang, Y Shi, X Zhang

Open access · goldAbstract read
In one paragraph

Article in European journal of histochemistry : EJH, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

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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

6 authors at 3 institutions in 2 countries.

H XuWannan Medical College. xuhg@maemail.com.cn.
X Zhang
H Wang
Y Zhang
Y Shi
X Zhang
Wannan Medical College · CNShanghai Jiao Tong University · CNWashington University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The normal ANK protein has a strong influence on anti-calcification. It is known that TGF-β1 is also able to induce extracellular inorganic pyrophosphate (ePPi) elaboration via the TGF-β1-induced ank gene expression and the mitogen-activated protein kinase (MAPK) signaling acts as a downstream effector of TGF-β1. We hypothesized that the expression of the ank gene is regulated by mechanics through TGF-β1-p38 pathway. In this study, we investigated the mechanism of short-time mechanical tension-induced ank gene expression. We found that the continuous cyclic mechanical tension (CCMT) increased the ank gene expression in the endplate chondrocytes, and there was an increase in the TGF-β1 expression after CCMT stimulation. The ank gene expression significantly increased when treated by TGF-β1 in a dose-dependent manner and decreased when treated by SB431542 (ALK inhibitor) in a dose-dependent manner. Our study results indicate that CCMT-induced ank gene expressions may be regulated by TGF-β1 and p38 MAPK pathway.

Indexed as

Torsion, MechanicalAnimalsCell SurvivalChondrocytesEnzyme-Linked Immunosorbent AssayGene Expression RegulationMAP Kinase Signaling SystemPhosphate Transport ProteinsRatsRats, Sprague-DawleyReal-Time Polymerase Chain ReactionTransforming Growth Factor beta1Ankh protein, mousePhosphate Transport ProteinsTransforming Growth Factor beta1

Identifiers

PMID24085277
PMCPMC3794359
OpenAlexW2121060449

What OpenQuestion holds

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LicenceCC BY-NC
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.