Evidence map›Paper›PMID 28493442›Full record

ArticleImmunity, inflammation and disease2017

uPA-derived peptide, Å6 is involved in the suppression of lipopolysaccaride-promoted inflammatory osteoclastogenesis and the resultant bone loss.

Yosuke Kanno, Chihiro Maruyama, Ayaka Matsuda, Akira Ishisaki

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.1field-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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Lipopolysaccharide-Induced Bone Loss in Rodent Models: A Systematic Review and Meta-Analysis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023
    Pooled it
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  10. Therapeutics targeting the fibrinolytic system.Experimental & molecular medicine · 2020
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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

4 authors at 2 institutions in 1 country.

Yosuke KannoFaculty of Pharmaceutical Science, Department of Clinical Pathological Biochemistry, Doshisha Women's Collage of Liberal Arts, Kyoto, Japan.ORCID 0000-0001-9741-2113
Chihiro MaruyamaFaculty of Pharmaceutical Science, Department of Clinical Pathological Biochemistry, Doshisha Women's Collage of Liberal Arts, Kyoto, Japan.
Ayaka MatsudaFaculty of Pharmaceutical Science, Department of Clinical Pathological Biochemistry, Doshisha Women's Collage of Liberal Arts, Kyoto, Japan.
Akira IshisakiDepartment of Biochemistry, Iwate Medical University School of Dentistry, Morioka, Iwate, Japan.
Doshisha Women's College of Liberal Arts · JPIwate Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionChronic inflammatory diseases such as rheumatoid arthritis and periodontitis frequently cause bone destruction. Inflammation-induced bone loss results from the increase of bone-resorbing osteoclasts. Recently, we demonstrated that urokinase type plasminogen activator (uPA) suppressed lipopolysaccaride (LPS)-inflammatory osteoclastogenesis through the adenosine monophosphate-activated protein kinase (AMPK) pathway, whereas its receptor (uPAR) promoted that through the Akt pathway.

methodsWe investigated the effects of uPA-derived peptide (Å6) in the LPS-induced inflammatory osteoclastogenesis and bone destruction.

resultsWe found that Å6 attenuated inflammatory osteoclastogenesis and bone loss induced by LPS in mice. We also showed that Å6 attenuated the LPS-promoted inflammatory osteoclastogenesis by inactivation of NF-κB in RAW264.7 mouse monocyte/macrophage lineage cells. Furthermore, we showed that Å6 attenuated the Akt phosphorylation, and promoted the AMPK phosphorylation.

conclusionÅ6 is involved in the suppression of LPS-promoted inflammatory osteoclastgensis and bone destruction by regulating the AMPK and Akt pathways. These findings provide a basis for clinical strategies to improve the bone loss caused by inflammatory diseases.

Indexed as

AMP-Activated Protein KinasesAnimalsBone ResorptionLipopolysaccharidesMiceOsteoclastsPeptidesProto-Oncogene Proteins c-aktSignal TransductionUrokinase-Type Plasminogen ActivatorAMP-Activated Protein Kinaseslipopolysaccharide, Escherichia coli O111 B4LipopolysaccharidesPeptidesProto-Oncogene Proteins c-aktUrokinase-Type Plasminogen ActivatorBone lossosteoclastsuPA-derived peptide Å6

Identifiers

PMID28493442
PMCPMC5569370
OpenAlexW2612160754

What OpenQuestion holds

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LicenceCC BY
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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.