Evidence map›Paper›PMID 25546513›Full record

ArticleThe spine journal : official journal of the North American Spine Society2015

Functional impact of integrin α5β1 on the homeostasis of intervertebral discs: a study of mechanotransduction pathways using a novel dynamic loading organ culture system.

Takuto Kurakawa, Kenichiro Kakutani, Yusuke Morita, Yuki Kato, Takashi Yurube, Hiroaki Hirata, Shingo Miyazaki, Yoshiki Terashima, Koichiro Maeno, Toru Takada and 5 more

Open access · greenAbstract read
In one paragraph

Article in The spine journal : official journal of the North American Spine Society, 2015. 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
2.1field-weighted citation impact, top 14% 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, 43 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

15 authors at 4 institutions in 2 countries.

Takuto KurakawaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyōgo Prefecture 657-8501, Japan.
Kenichiro KakutaniDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyōgo Prefecture 657-8501, Japan. Electronic address: kenkakutani@gmail.com.
Yusuke MoritaDepartment of Biomedical Engineering, Doshisha University, Karasuma-Higashi-iru, Kyoto, Kyoto Prefecture 602-8580, Japan.
Yuki KatoDepartment of Biomedical Engineering, Doshisha University, Karasuma-Higashi-iru, Kyoto, Kyoto Prefecture 602-8580, Japan.
Takashi YurubeDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyōgo Prefecture 657-8501, Japan.
Hiroaki HirataDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyōgo Prefecture 657-8501, Japan.
Shingo MiyazakiDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyōgo Prefecture 657-8501, Japan.
Yoshiki TerashimaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyōgo Prefecture 657-8501, Japan.
Koichiro MaenoDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyōgo Prefecture 657-8501, Japan.
Toru TakadaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyōgo Prefecture 657-8501, Japan.
Minoru DoitaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyōgo Prefecture 657-8501, Japan.
Masahiro KurosakaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyōgo Prefecture 657-8501, Japan.
Nozomu InoueDepartment of Biomedical Engineering, Doshisha University, Karasuma-Higashi-iru, Kyoto, Kyoto Prefecture 602-8580, Japan; Department of Orthopedic Surgery, Rush University Medical Center, 1653 W. Congress Parkway, Chicago, IL 60612, USA.
Koichi MasudaDepartment of Orthopaedic Surgery, University of California San Diego School of Medicine, 9500 Gilman Drive, La Jolla, San Diego, CA 92093, USA.
Kotaro NishidaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyōgo Prefecture 657-8501, Japan.
Kobe University · JPDoshisha University · JPRush University Medical Center · USUniversity of California San Diego · US

Funding

Segmental spine motion of the lumbar spineP01AR048152 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI MASUDA, KOICHI · 2001 to 2010
$13.7M
NIAMS NIH HHS P01 AR048152
6 · The paper itself

Abstract

background contextIntervertebral disc (IVD) degeneration, a major cause of low back pain, is considered to be induced by daily mechanical loading. Mechanical stress is widely known to affect cell survival and extracellular matrix metabolism in many cell types. Although the involvement of integrin α5β1 transmembrane mechanoreceptor in IVD degeneration has been reported, the precise function of integrin α5β1 remains obscure. PURPOSE: To reflect IVD tissue response to mechanical stress using a dynamic loading organ culture system and elucidate the functional impact of integrin α5β1 on the pathomechanism of IVD degeneration. STUDY

designAn ex vivo study using a dynamic loading organ culture system.

methodsNinety-six rat IVD explants were examined. Intervertebral discs were subjected to 1.3 MPa, 1.0 Hz dynamic compressive load in the presence or absence of an Arg-Gly-Asp (RGD) peptide with affinity to the fibronectin binding-site of integrin α5β1. Cell viability and histomorphology were assessed. The localization of integrin α5β1 in the IVD was assessed by immunohistochemistry. Gene expression levels of IVD cells were evaluated using real-time reverse transcription-polymerase chain reaction.

resultsIn the nucleus pulposus (NP), cell density and viability were reduced by dynamic compressive load. Histologic degenerative alterations, mainly seen in the NP, were the morphologic changes of NP cells. In both NP and annulus fibrosus (AF), immunohistochemistry revealed localization of integrin α5β1 and that the messenger-RNA expression of integrin α5β1 was increased by dynamic load. Dynamic load induced a catabolic effect, the stimulation of matrix metalloproteinase-3 and -13 gene expressions by NP and AF cells. The RGD peptide partially blocked the histologic alterations and the catabolic effect.

conclusionsThe dynamic loading organ culture system simulated cellular responses to mechanical loading of the IVD. Our results suggest that IVD cells recognize the mechanical stress through RGD integrins, particularly the α5β1 subtype that is highly expressed in NP and AF cells. Further experiments using this system will provide information about pathomechanisms of IVD degeneration through the mechanotransduction pathways.

Indexed as

Mechanotransduction, CellularAnimalsCell CountHomeostasisImmunohistochemistryIntegrin alpha5beta1Intervertebral DiscIntervertebral Disc DegenerationMatrix Metalloproteinase 3OligopeptidesOrgan Culture TechniquesRatsReal-Time Polymerase Chain ReactionStress, Mechanicalarginyl-glycyl-aspartic acidIntegrin alpha5beta1Matrix Metalloproteinase 3OligopeptidesCompressionIntegrinIntervertebral disc degenerationMechanical loadMechanoreceptorOrgan culture

Identifiers

PMID25546513
PMCPMC5673479
OpenAlexW2011724488

What OpenQuestion holds

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LicenceTDM
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.