Evidence map›Paper›PMID 26839464›Full record

ArticleMediators of inflammation2015

Gene Expression Profiling of IL-17A-Treated Synovial Fibroblasts from the Human Temporomandibular Joint.

Toshio Hattori, Naomi Ogura, Miwa Akutsu, Mutsumi Kawashima, Suguru Watanabe, Ko Ito, Toshirou Kondoh

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

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  12. The protective capability ofFrontiers in immunology · 2022
    Article
  13. Article
  14. Systemic effects of IL-17 in inflammatory arthritis.Nature reviews. Rheumatology · 2019
    Review
  15. Article
  16. Review
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

7 authors at 1 institution in 1 country.

Toshio HattoriDepartment of Maxillofacial Surgery, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba 271-8587, Japan.
Naomi OguraDepartment of Maxillofacial Surgery, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba 271-8587, Japan; Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba 271-8587, Japan.
Miwa AkutsuDepartment of Maxillofacial Surgery, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba 271-8587, Japan; Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba 271-8587, Japan.
Mutsumi KawashimaDepartment of Maxillofacial Surgery, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba 271-8587, Japan.
Suguru WatanabeDepartment of Maxillofacial Surgery, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba 271-8587, Japan.
Ko ItoDepartment of Maxillofacial Surgery, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba 271-8587, Japan; Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba 271-8587, Japan.
Toshirou KondohDepartment of Maxillofacial Surgery, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba 271-8587, Japan; Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba 271-8587, Japan.
Nihon University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synovial fibroblasts contribute to the inflammatory temporomandibular joint under pathogenic stimuli. Synovial fibroblasts and T cells participate in the perpetuation of joint inflammation in a mutual activation feedback, via secretion of cytokines and chemokines that stimulate each other. IL-17 is an inflammatory cytokine produced primarily by Th17 cells which plays critical role in the pathogenesis of numerous autoimmune and inflammatory diseases. Here, we investigated the roles of IL-17A in temporomandibular joint disorders (TMD) using genome-wide analysis of synovial fibroblasts isolated from patients with TMD. IL-17 receptors were expressed in synovial fibroblasts as assessed using real-time PCR. Microarray analysis indicated that IL-17A treatment of synovial fibroblasts upregulated the expression of IL-6 and chemokines. Real-time PCR analysis showed that the gene expression of IL-6, CXCL1, IL-8, and CCL20 was significantly higher in IL-17A-treated synovial fibroblasts compared to nontreated controls. IL-6 protein production was increased by IL-17A in a time- and a dose-dependent manner. Additionally, IL-17A simulated IL-6 protein production in synovial fibroblasts samples isolated from three patients. Furthermore, signal inhibitor experiments indicated that IL-17-mediated induction of IL-6 was transduced via activation of NFκB and phosphatidylinositol 3-kinase/Akt. These results suggest that IL-17A is associated with the inflammatory progression of TMD.

Indexed as

Gene Expression ProfilingAdultCells, CulturedFemaleFibroblastsHumansInterleukin-17Interleukin-6MaleMiddle AgedReceptors, Interleukin-17Signal TransductionSynovial MembraneTemporomandibular JointTemporomandibular Joint DisordersIL6 protein, humanInterleukin-17Interleukin-6Receptors, Interleukin-17

Identifiers

PMID26839464
PMCPMC4709758
OpenAlexW2267192332

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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.