Evidence map›Paper›PMID 35661290›Full record

ArticleJournal of molecular histology2022

IL-6 promotes low concentration of RANKL-induced osteoclastic differentiation by mouse BMMs through trans-signaling pathway.

Wei Feng, Panpan Yang, Hongrui Liu, Fan Zhang, Minqi Li

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular histology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 22 citations in OpenAlex.

  1. S100A9 Induces RANKL Expression in Osteocytes Utilizing IL-6/sIL-6R Combination and gp130 Signaling Pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Frontiers in pharmacology · 2026
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Bone-muscle crosstalk under physiological and pathological conditions.Cellular and molecular life sciences : CMLS · 2024
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

5 authors at 2 institutions in 1 country.

Wei FengDepartment of Endodontics, Central Laboratory of Jinan Stomatological Hospital, Jinan Key Laboratory of Oral Tissue Regeneration, 250001, Jinan, Shandong, China.
Panpan YangCenter of Osteoporosis and Bone Mineral Research, Shandong University, 250012, Jinan, Shandong, China.
Hongrui LiuCenter of Osteoporosis and Bone Mineral Research, Shandong University, 250012, Jinan, Shandong, China.
Fan ZhangCenter of Osteoporosis and Bone Mineral Research, Shandong University, 250012, Jinan, Shandong, China.ORCID http://orcid.org/0000-0002-9612-5638
Minqi LiCenter of Osteoporosis and Bone Mineral Research, Shandong University, 250012, Jinan, Shandong, China. liminqi@sdu.edu.cn.ORCID http://orcid.org/0000-0001-9980-1382
Shandong University · CNJinan Stomatological Hospital · CN

Funding

Construction Engineering Special Fund of "Taishan Scholars" of Shandong Province tsqn202103177he Key Research and Development Program of Shandong Province 2019GSF107016National Natural Science Foundation of China 81800982National Natural Science Foundation of China 81972072the Open Foundation of Shandong Province Key Laboratory of Oral Tissue Regeneration SDKQ201703
6 · The paper itself

Abstract

The exact role of IL-6 in inflammatory osteoclast formation is still under debate. Our previous study demonstrated that IL-6 in the combination of sIL-6R significantly promoted low level of RANKL-induced osteoclast differentiation which was not affected by IL-6 alone. However, the precise molecular mechanisms underlying the regulation of sIL-6R-induced trans-signaling on osteoclast differentiation remains to be elucidated. Mouse bone marrow‑derived monocytes (BMMs) were isolated and cultured with RANKL and IL-6/sIL-6R in the presence or absence of sgp130. TRAP staining and pit formation assay were used to visualize multinucleated giant osteoclasts and evaluate their bone resorption ability. Western blot and real time-PCR were applied to determine the activations of IL-6 signaling pathway and osteoclastogenesis- associated signaling pathways. The results showed that sIL-6R activation of IL-6 trans-signaling enhanced IL-6 signaling cascades and promoted low concentration of RANKL-induced osteoclasts formation and bone resorption by mouse BMMs. Furthermore, blocking IL-6 trans-signaling with sgp130 abrogated this promotive effect by suppressing NF-κB and JNK signaling pathways. In conclusion, sIL-6R-mediated trans-signaling pathway plays a decisive role in promotion of low level of RANKL-induced osteoclastic differentiation by IL-6/sIL-6R and targeting the IL-6 trans-signaling pathway may represent a potential strategy for inflammatory diseases with pathological bone resorption.

Indexed as

Bone ResorptionInterleukin-6AnimalsCell DifferentiationCytokine Receptor gp130MiceMonocytesOsteoclastsRANK LigandSignal TransductionCytokine Receptor gp130Interleukin-6RANK LigandIL-6Osteoclastsgp130sIL-6RTrans-signaling

Identifiers

PMID35661290
OpenAlexW4281878436

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.