Evidence map›Paper›PMID 26805019›Full record

ArticleOsteoarthritis and cartilage2016

MicroRNA-155 suppresses autophagy in chondrocytes by modulating expression of autophagy proteins.

S D'Adamo, O Alvarez-Garcia, Y Muramatsu, F Flamigni, M K Lotz

Abstract 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 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

60 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Guideline
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  7. Forkhead box O proteins in chondrocyte aging and diseases.Journal of orthopaedic translation · 2025
    Review
  8. Article
  9. Article
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  11. Article
  12. Review
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  14. Article
  15. Review
  16. Article
  17. Chondrocyte autophagy mechanism and therapeutic prospects in osteoarthritis.Frontiers in cell and developmental biology · 2024
    Review
  18. Review
  19. 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

5 authors.

S D'AdamoDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA, USA; Department of Biomedical and Neuromotor Sciences, University of Bologna, Italy.
O Alvarez-GarciaDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA, USA.
Y MuramatsuDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA, USA.
F FlamigniDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Italy.
M K LotzDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA, USA. Electronic address: mlotz@scripps.edu.

Funding

TISSUE ACQUISITION, MORPHOLOGY, AND CELL CULTUREP01AG007996 · NIA · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI SAH, ROBERT L · 1989 to 2016
$26.0M
Integrative Omics analysis of human cartilage in aging and osteoarthritisR01AG049617 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI LOTZ, MARTIN K · 2016 to 2024
$5.6M
NIA NIH HHS P01 AG007996NIA NIH HHS R01 AG049617
6 · The paper itself

Abstract

objectiveAutophagy dysfunction has been reported in osteoarthritis (OA) cartilage. The objective of this study was to investigate the role of microRNA-155 (miR-155), which is overexpressed in OA, in the regulation of autophagy in human chondrocytes.

designRapamycin (50 nM) and 2-deoxyglucose (2-DG) (5 mM) were used to stimulate autophagy in primary human articular chondrocytes and in the T/C28a2 human chondrocyte cell line. Cells were transfected with LNA GapmeR or mimic specific for miR-155 and autophagy flux was assessed by LC3 western blotting and by Cyto-ID(®) dye quantification in autophagic vacuoles. Expression of predicted miR-155 targets in the autophagy pathway were analyzed by real-time PCR and western blotting.

resultsAutophagy flux induced by rapamycin and 2-DG was significantly increased by miR-155 LNA, and significantly decreased after miR-155 mimic transfection in T/C28a2 cells and in human primary chondrocytes. These effects of miR-155 on autophagy were related to suppression of gene and protein expression of key autophagy regulators including Ulk1, FoxO3, Atg14, Atg5, Atg3, Gabarapl1, and Map1lc3.

conclusionMiR-155 is an inhibitor of autophagy in chondrocytes and contributes to the autophagy defects in OA.

Indexed as

AutophagyCartilage, ArticularCells, CulturedChondrocytesHumansMicroRNAsOsteoarthritisMicroRNAsAutophagyCartilageChondrocytesmicroRNAs

Identifiers

PMID26805019
PMCPMC4875787

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Registered trials

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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.