Evidence map›Paper›PMID 35101442›Full record

ArticleThe Journal of biological chemistry2022

Endosomal TLR3 signaling in stromal osteoblasts induces prostaglandin E

Tsukasa Tominari, Miyuki Akita, Chiho Matsumoto, Michiko Hirata, Shosei Yoshinouchi, Yuki Tanaka, Kento Karouji, Yoshifumi Itoh, Takayuki Maruyama, Chisato Miyaura and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 10 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

12 authors at 4 institutions in 2 countries.

Tsukasa TominariDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan.
Miyuki AkitaDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan.
Chiho MatsumotoDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan.
Michiko HirataDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan.
Shosei YoshinouchiCooperative Major of Advanced Health Science, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan.
Yuki TanakaDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan.
Kento KaroujiDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan.
Yoshifumi ItohInstitute of Global Innovation Research, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan; Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Kennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
Takayuki MaruyamaMinase Research Institutes, Ono Pharmaceutical Co Ltd, Osaka, Japan.
Chisato MiyauraDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan; Cooperative Major of Advanced Health Science, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan; Institute of Global Innovation Research, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan.
Yukihiro NumabeDepartment of Periodontology, School of Dentistry, The Nippon Dental University, Chiyoda-ku, Tokyo, Japan.
Masaki InadaDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan; Cooperative Major of Advanced Health Science, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan; Institute of Global Innovation Research, Tokyo University of Agriculture and Technology, Koganei, Tokyo, Japan. Electronic address: m-inada@cc.tuat.ac.jp.
Tokyo University of Agriculture and Technology · JPNippon Dental University · JPNuffield Orthopaedic Centre · GBOno Pharmaceutical (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptors (TLRs) are pattern recognition receptors that play a critical role in innate immune diseases. TLR3, which is localized in the endosomal compartments of hematopoietic immune cells, is able to recognize double-stranded RNA (dsRNA) derived from viruses and bacteria and thereby induce innate immune responses. Inflammatory periodontal bone resorption is caused by bacterial infections, which initially is regulated by innate immunity; however, the roles of TLR3 signaling in bone resorption are still not known. We examined the roles of TLR3 signaling in bone resorption using poly(I:C), a synthetic dsRNA analog. In cocultures of mouse bone marrow cells and stromal osteoblasts, poly(I:C) clearly induced osteoclast differentiation. In osteoblasts, poly(I:C) increased PGE

Indexed as

Bone ResorptionDinoprostoneOsteoblastsToll-Like Receptor 3AnimalsCells, CulturedEndosomesIndomethacinMiceOsteoclastsProstaglandins ERANK LigandRNA, MessengerDinoprostoneIndomethacinProstaglandins ERANK LigandRNA, MessengerTLR3 protein, mouseToll-Like Receptor 3bone resorptionosteoblastosteoclastprostaglandinToll-like receptor

Identifiers

PMID35101442
PMCPMC8892075
OpenAlexW4210280410

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.