Evidence map›Paper›PMID 26493329›Full record

ArticleOsteoarthritis and cartilage2016

IFT88 influences chondrocyte actin organization and biomechanics.

Z Wang, A K T Wann, C L Thompson, A Hassen, W Wang, M M Knight

Open access · hybridAbstract read
In one paragraph

Article in Osteoarthritis and cartilage, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Ciliary and Non-Ciliary Roles of IFT88 in Development and Diseases.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Primary cilium-mediated mechanotransduction in cartilage chondrocytes.Experimental biology and medicine (Maywood, N.J.) · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. Ciliary IFT88 Protects Coordinated Adolescent Growth Plate Ossification From Disruptive Physiological Mechanical Forces.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Article
  11. Review
  12. Mitral Valve Prolapse Induces Regionalized Myocardial Fibrosis.Journal of the American Heart Association · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

6 authors at 2 institutions in 1 country.

Z WangInstitute of Bioengineering and School of Engineering and Materials Science, Queen Mary University of London, London, United Kingdom.
A K T WannKennedy Institute of Rheumatology, University of Oxford, Oxford, United Kingdom.
C L ThompsonInstitute of Bioengineering and School of Engineering and Materials Science, Queen Mary University of London, London, United Kingdom. Electronic address: clare.l.thompson@qmul.ac.uk.
A HassenInstitute of Bioengineering and School of Engineering and Materials Science, Queen Mary University of London, London, United Kingdom.
W WangInstitute of Bioengineering and School of Engineering and Materials Science, Queen Mary University of London, London, United Kingdom.
M M KnightInstitute of Bioengineering and School of Engineering and Materials Science, Queen Mary University of London, London, United Kingdom.
Queen Mary University of London · GBUniversity of Oxford · GB

Funding

Biotechnology and Biological Sciences Research Council E17114Medical Research Council MR/L002876/1Versus Arthritis 19830
6 · The paper itself

Abstract

objectivesPrimary cilia are microtubule based organelles which control a variety of signalling pathways important in cartilage development, health and disease. This study examines the role of the intraflagellar transport (IFT) protein, IFT88, in regulating fundamental actin organisation and mechanics in articular chondrocytes.

methodsThe study used an established chondrocyte cell line with and without hypomorphic mutation of IFT88 (IFT88(orpk)). Confocal microscopy was used to quantify F-actin and myosin IIB organisation. Viscoelastic cell and actin cortex mechanics were determined using micropipette aspiration with actin dynamics visualised in live cells transfected with LifeACT-GFP.

resultsIFT88(orpk) cells exhibited a significant increase in acto-myosin stress fibre organisation relative to wild-type (WT) cells in monolayer and an altered response to cytochalasin D. Rounded IFT88(orpk) cells cultured in suspension exhibited reduced cortical actin expression with reduced cellular equilibrium modulus. Micropipette aspiration resulted in reduced membrane bleb formation in IFT88(orpk) cells. Following membrane blebbing, IFT88(orpk) cells exhibited slower reformation of the actin cortex. IFT88(orpk) cells showed increased actin deformability and reduced cortical tension confirming that IFT regulates actin cortex mechanics. The reduced cortical tension is also consistent with the reduced bleb formation.

conclusionsThis study demonstrates for the first time that the ciliary protein IFT88 regulates fundamental actin organisation and the stiffness of the actin cortex leading to alterations in cell deformation, mechanical properties and blebbing in an IFT88 chondrocyte cell line. This adds to the growing understanding of the role of primary cilia and IFT in regulating cartilage biology.

Indexed as

ActinsAnimalsCartilage, ArticularCells, CulturedCell ShapeChondrocytesCiliaCytochalasin DElasticityMice, Mutant StrainsMutationNonmuscle Myosin Type IIBSignal TransductionTumor Suppressor ProteinsViscosityActinsCytochalasin DNonmuscle Myosin Type IIBTg737Rpw protein, mouseTumor Suppressor ProteinsCell mechanicsF-actinITF88Micropipette aspirationMyosin IIB

Identifiers

PMID26493329
PMCPMC4769095
OpenAlexW2173239974

What OpenQuestion holds

Textmetadata
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.