Evidence map›Paper›PMID 26634249›Full record

ArticleArthritis research & therapy2015

High level of interleukin-32 gamma in the joint of ankylosing spondylitis is associated with osteoblast differentiation.

Eun-Ju Lee, Eun-Jin Lee, Yeon-Ho Chung, Da-Hyun Song, Seokchan Hong, Chang-Keun Lee, Bin Yoo, Tae-Hwan Kim, Ye-Soo Park, Soo-Hyun Kim and 2 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.9field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

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  14. Osteoblast Role in Rheumatic Diseases.International journal of molecular sciences · 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

12 authors at 4 institutions in 1 country.

Eun-Ju LeeDepartment of Rheumatology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43 gil, Songpa-gu, Seoul, 05505, Korea. krys72@hanmail.net.
Eun-Jin LeeDepartment of Biomedical Sciences, Cell Dysfunction Research Center and BMIT, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43 gil, Songpa-gu, Seoul, 05505, Korea. ejlee09@gmail.com.
Yeon-Ho ChungDepartment of Biomedical Sciences, Cell Dysfunction Research Center and BMIT, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43 gil, Songpa-gu, Seoul, 05505, Korea. rcn-2xx@hanmail.net.
Da-Hyun SongDepartment of Biomedical Sciences, Cell Dysfunction Research Center and BMIT, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43 gil, Songpa-gu, Seoul, 05505, Korea. astrony_@nate.com.
Seokchan HongDepartment of Rheumatology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43 gil, Songpa-gu, Seoul, 05505, Korea. hongsc97@hanmail.net.
Chang-Keun LeeDepartment of Rheumatology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43 gil, Songpa-gu, Seoul, 05505, Korea. cklee@amc.seoul.kr.
Bin YooDepartment of Rheumatology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43 gil, Songpa-gu, Seoul, 05505, Korea. byoo@amc.seoul.kr.
Tae-Hwan KimDepartment of Rheumatology, Hanyang University Hospital for Rheumatic Diseases, Seoul, 133-791, Korea. thkim@hanyang.ac.kr.
Ye-Soo ParkDepartment of Orthopaedic Surgery, Guri Hospital, Hanyang University College of Medicine, Kyunggi-do, 471-701, Korea. hyparkys@hanyang.ac.kr.
Soo-Hyun KimDepartment of Biomedical Science and Technology, Konkuk University, Seoul, 143-701, Korea. soohyun@konkuk.ac.kr.
Eun-Ju ChangDepartment of Biomedical Sciences, Cell Dysfunction Research Center and BMIT, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43 gil, Songpa-gu, Seoul, 05505, Korea. ejchang@amc.seoul.kr.
Yong-Gil KimDepartment of Rheumatology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43 gil, Songpa-gu, Seoul, 05505, Korea. bestmd2000@amc.seoul.kr.
Ulsan College · KRUniversity of Ulsan · KRHanyang University Seoul Hospital · KRKonkuk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgoundThe formation of bony spurs and ankylosis is a key pathognomic feature in ankylosing spondylitis (AS) and results in functional impairment. The aim of this study was to investigate the role of IL-32γ in osteoblast (OB) differentiation and its association with the pathogenesis of AS.

methodsThe concentration and expression of IL-32γ were evaluated in synovial fluid and tissue from patients with AS, rheumatoid arthritis (RA) and osteoarthritis (OA), using enzyme-linked immunosorbent assay and immunohistochemistry. To establish whether IL-32γ affects OB differentiation, we used calvarial cells of IL-32γ transgenic (TG) mice or wild-type (WT) mice. To elucidate the mechanism of osteoblastogenesis, levels of regulators were assayed in IL-32γ TG mice and in primary OBs after IL-32γ stimulation.

resultsThe IL-32γ levels were higher in the synovial fluid of AS patients compared with RA or OA patients and the expression of IL-32 was higher in AS synovia than in RA or OA synovia. Additional IL-32γ stimulation in precursor cells enhanced OB differentiation potentially and IL-32γ TG mice showed higher rates of OB differentiation than WT mice. IL-32γ reduced the expression of DKK-1, a negative regulator, in both WT precursor cells and human OBs and the constitutive expression of DKK-1 was suppressed in calvarial cells from IL-32γ TG mice.

conclusionsThe elevated level of IL-32γ in AS joint could enhance OB differentiation via DKK-1 suppression. Therefore, IL-32γ might be a putative molecular target to prevent the abnormal bone formation in AS.

Indexed as

AnimalsBlotting, WesternCell DifferentiationEnzyme-Linked Immunosorbent AssayHumansImmunohistochemistryInterleukinsMiceMice, Inbred C57BLMice, TransgenicOsteoblastsReverse Transcriptase Polymerase Chain ReactionSpondylitis, AnkylosingSynovial FluidSynovial MembraneIL32 protein, humaninterleukin-32, mouseInterleukins

Identifiers

PMID26634249
PMCPMC4669668
OpenAlexW2187414530

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LicenceCC BY
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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.