Evidence map›Paper›PMID 21181166›Full record

ArticleRheumatology international2011

Proinflammatory cytokines, IL-1β and TNF-α, induce expression of interleukin-34 mRNA via JNK- and p44/42 MAPK-NF-κB pathway but not p38 pathway in osteoblasts.

Hiroyuki Eda, Hideaki Shimada, David R Beidler, Joseph B Monahan

Abstract read
PubMed Publisher
In one paragraph

Article in Rheumatology international, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 101 citations in OpenAlex.

  1. Review
  2. Review
  3. Frontiers in veterinary science · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Targeting IL-34/MCSF-1R Axis in Colon Cancer.Frontiers in immunology · 2022
    Review
  8. Article
  9. Resveratrol-Induced Signal Transduction in Wound Healing.International journal of molecular sciences · 2021
    Review
  10. Review
  11. Article
  12. Increased Levels of IL-34 in Acquired Immune-Mediated Neuropathies.Journal of molecular neuroscience : MN · 2021
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. G2A AttenuatesAnnals of dermatology · 2017
    Article
  20. 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

4 authors at 2 institutions in 1 country.

Hiroyuki EdaDiscovery Biology, Global Research and Development, St. Louis Laboratories, Pfizer Inc., 700 Chesterfield Parkway West, mail zone AA3C, Chesterfield, MO 63017, USA. hiroyuki_eda@ajinomoto.com
Hideaki Shimada
David R Beidler
Joseph B Monahan
Pfizer (United States) · USAjinomoto (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study is to investigate the induction of interleukin-34 (IL-34) and macrophage colony-stimulating factor (M-CSF) mRNA by inflammatory cytokines and the involvement of mitogen-activated protein kinases (MAPKs) in this signaling pathway in human osteoblasts as both IL-34 and M-CSF bind to the same receptor c-FMS. Among four inflammatory cytokines [(IL-1β, IL-6, IL-17, and tumor necrosis factor-α (TNF-α)], IL-34 mRNA expression level was dramatically induced by IL-1β (17-fold) and TNF-α (74-fold). IL-1β and TNF-α activated the intracellular mitogen-activated protein kinases (MAPKs): p44/42 MAPK, p38, and c-Jun N-terminal kinase (JNK) as well as nuclear factor-κB (NF-κB) in osteoblasts. IL-1β- and TNF-α-mediated induction of IL-34 mRNA expression was decreased by JNK inhibitor. Interestingly, although treatment of MEK-1/2 inhibitor showed no reduction in the increase of IL-34 mRNA expression by cytokines, combination of MEK-1/2 inhibitor and JNK inhibitor significantly inhibited IL-1β- and TNF-α-mediated IL-34 mRNA expression level compared to those by each inhibitor alone. On the other hand, M-CSF mRNA expression level was significantly induced by both IL-1β and TNF-α by up to 7- and 11-fold, respectively. IL-1β- and TNF-α-mediated induction of M-CSF mRNA was not affected by p38, JNK, and MEK-1/2 inhibitors. However, NF-κB inhibitor completely inhibited the elevation of M-CSF mRNA expression by these cytokines. These results showed that proinflammatory cytokines, IL-1β and TNF-α, induced the expression of IL-34 mRNA via JNK and p44/42 MAPK but not p38 in human osteoblasts while p38, JNK, and p44/42 MAPK were not involved in the induction of M-CSF mRNA expression by these cytokines.

Indexed as

Cells, CulturedCytokinesEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesGene Expression RegulationHumansInterleukin-1betaInterleukinsJNK Mitogen-Activated Protein KinasesMacrophage Colony-Stimulating FactorMAP Kinase Signaling SystemMitogen-Activated Protein KinasesNF-kappa BOsteoblastsRNA, MessengerSignal TransductionCytokinesEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesIL34 protein, humanInterleukin-1betaInterleukinsJNK Mitogen-Activated Protein KinasesMacrophage Colony-Stimulating FactorMitogen-Activated Protein KinasesNF-kappa BRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID21181166
OpenAlexW2114691515

What OpenQuestion holds

Textmetadata
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.