Evidence map›Paper›PMID 25470448›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2015

Loss of SH3 domain-binding protein 2 function suppresses bone destruction in tumor necrosis factor-driven and collagen-induced arthritis in mice.

Tomoyuki Mukai, Richard Gallant, Shu Ishida, Mizuho Kittaka, Teruhito Yoshitaka, David A Fox, Yoshitaka Morita, Keiichiro Nishida, Robert Rottapel, Yasuyoshi Ueki

Open access · greenAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

28 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Loss-of-functionJBMR plus · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Effect of microRNA-663b on migration, invasion and epithelial‑mesenchymal transition of oral squamous cell carcinoma cells.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. TRAPS mutations inFrontiers in immunology · 2022
    Article
  14. SH3BP2 Deficiency Ameliorates Murine Systemic Lupus Erythematosus.International journal of molecular sciences · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Alveolar Bone Protection by Targeting the SH3BP2-SYK Axis in Osteoclasts.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020
    Article
  19. Article
  20. Cells · 2019
    Article
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

10 authors at 5 institutions in 3 countries.

Tomoyuki MukaiUniversity of Missouri-Kansas City.
Richard Gallant
Shu Ishida
Mizuho Kittaka
Teruhito Yoshitaka
David A Fox
Yoshitaka Morita
Keiichiro Nishida
Robert Rottapel
Yasuyoshi Ueki
University of Missouri–Kansas City · USKawasaki Medical School · JPOkayama University · JPSt. Michael's Hospital · CAUniversity of Michigan–Ann Arbor · US

Funding

Molecular and Cellular Pathogenesis of CherubismR01DE020835 · NIDCR · UNIVERSITY OF MISSOURI KANSAS CITY · PI UEKI, YASUYOSHI · 2010 to 2014
$1.8M
NIDCR NIH HHS R01 DE020835NIDCR NIH HHS R01-DE-020835
6 · The paper itself

Abstract

objectiveSH3 domain-binding protein 2 (SH3BP2) is a signaling adapter protein that regulates the immune and skeletal systems. The present study was undertaken to investigate the role of SH3BP2 in arthritis using 2 experimental mouse models, i.e., human tumor necrosis factor α-transgenic (hTNF-Tg) mice and mice with collagen-induced arthritis (CIA).

methodsFirst, Sh3bp2(-/-) and wild-type (Sh3bp2(+/+) ) mice were crossed with hTNF-Tg mice. Inflammation and bone loss were examined by clinical inspection and histologic and micro-computed tomography analysis, and osteoclastogenesis was evaluated using primary bone marrow-derived macrophage colony-stimulating factor-dependent macrophages (BMMs). Second, CIA was induced in Sh3bp2(-/-) and Sh3bp2(+/+) mice, and the incidence and severity of arthritis were evaluated. Anti-mouse type II collagen (CII) antibody levels were measured by enzyme-linked immunosorbent assay, and lymph node cell responses to CII were determined.

resultsSH3BP2 deficiency did not alter the severity of joint swelling but did suppress bone erosion in the hTNF-Tg mouse model. Bone loss at the talus and tibia was prevented in Sh3bp2(-/-) /hTNF-Tg mice compared to Sh3bp2(+/+) /hTNF-Tg mice. RANKL- and TNFα-induced osteoclastogenesis was suppressed in Sh3bp2(-/-) mouse BMM cultures. NF-ATc1 nuclear localization in response to TNFα was decreased in Sh3bp2(-/-) mouse BMMs compared to Sh3bp2(+/+) mouse BMMs. In the CIA model, SH3BP2 deficiency suppressed the incidence of arthritis and this was associated with decreased anti-CII antibody production, while antigen-specific T cell responses in lymph nodes were not significantly different between Sh3bp2(+/+) and Sh3bp2(-/-) mice.

conclusionSH3BP2 deficiency prevents loss of bone via impaired osteoclastogenesis in the hTNF-Tg mouse model and suppresses the induction of arthritis via decreased autoantibody production in the CIA model. Therefore, SH3BP2 could potentially be a therapeutic target in rheumatoid arthritis.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsArthritis, ExperimentalAutoantibodiesBlotting, WesternBone ResorptionCollagen Type IIEnzyme-Linked Immunosorbent AssayHumansMiceMice, Inbred C57BLMice, TransgenicNFATC Transcription FactorsOsteoclastsReal-Time Polymerase Chain ReactionRNA, MessengerAdaptor Proteins, Signal TransducingAutoantibodiesCollagen Type IINFATC Transcription FactorsRNA, MessengerSh3bp2 protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID25470448
PMCPMC4342302
OpenAlexW1939106472

What OpenQuestion holds

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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.