Evidence map›Paper›PMID 22481441›Full record

ArticleCellular and molecular life sciences : CMLS2012

Primary cilia elongation in response to interleukin-1 mediates the inflammatory response.

A K T Wann, M M Knight

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

88 citing papers in PubMed, 135 citations in OpenAlex.

  1. The F-Actin of In Situ Chondrocytes in Non-Degenerate and Mildly-Degenerate Human Cartilage: Changes With Cell Volume, and Cytoplasmic Processes.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026
    Article
  2. Article
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  5. Ciliary-Mediated Mechanotransduction in Skeletal Development and Diseases.Results and problems in cell differentiation · 2026
    Review
  6. Article
  7. Article
  8. Ciliary and Non-Ciliary Roles of IFT88 in Development and Diseases.International journal of molecular sciences · 2025
    Review
  9. Review
  10. Air Pollution and Osteoporosis.Current osteoporosis reports · 2024
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
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  17. Review
  18. Article
  19. ALS-linked C9orf72-SMCR8 complex is a negative regulator of primary ciliogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  20. Article

28 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

A K T WannBiomedical Engineering, 2nd Floor Cell and Tissue Laboratories, School of Engineering and Materials Science, Queen Mary, University of London, Mile End Road, London, E1 4NS, UK. a.wann@qmul.ac.uk
M M Knight
Queen Mary University of London · GB

Funding

Arthritis Research UKWellcome Trust
6 · The paper itself

Abstract

Primary cilia are singular, cytoskeletal organelles present in the majority of mammalian cell types where they function as coordinating centres for mechanotransduction, Wnt and hedgehog signalling. The length of the primary cilium is proposed to modulate cilia function, governed in part by the activity of intraflagellar transport (IFT). In articular cartilage, primary cilia length is increased and hedgehog signaling activated in osteoarthritis (OA). Here, we examine primary cilia length with exposure to the quintessential inflammatory cytokine interleukin-1 (IL-1), which is up-regulated in OA. We then test the hypothesis that the cilium is involved in mediating the downstream inflammatory response. Primary chondrocytes treated with IL-1 exhibited a 50% increase in cilia length after 3 h exposure. IL-1-induced cilia elongation was also observed in human fibroblasts. In chondrocytes, this elongation occurred via a protein kinase A (PKA)-dependent mechanism. G-protein coupled adenylate cyclase also regulated the length of chondrocyte primary cilia but not downstream of IL-1. Chondrocytes treated with IL-1 exhibit a characteristic increase in the release of the inflammatory chemokines, nitric oxide and prostaglandin E2. However, in cells with a mutation in IFT88 whereby the cilia structure is lost, this response to IL-1 was significantly attenuated and, in the case of nitric oxide, completely abolished. Inhibition of IL-1-induced cilia elongation by PKA inhibition also attenuated the chemokine response. These results suggest that cilia assembly regulates the response to inflammatory cytokines. Therefore, the cilia proteome may provide a novel therapeutic target for the treatment of inflammatory pathologies, including OA.

Indexed as

AnimalsCattleCells, CulturedChondrocytesCiliaCyclic AMP-Dependent Protein KinasesDinoprostoneFibroblastsFluorescent Antibody TechniqueHumansInflammationInterleukin-1betaNitric OxideSignal TransductionTumor Suppressor ProteinsCyclic AMP-Dependent Protein KinasesDinoprostoneIFT88 protein, humanInterleukin-1betaNitric OxideTumor Suppressor Proteins

Identifiers

PMID22481441
PMCPMC3417094
OpenAlexW2012956265

What OpenQuestion holds

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LicenceCC BY
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.