Evidence map›Paper›PMID 32407895›Full record

ArticleOsteoarthritis and cartilage2020

tRNA-derived fragments (tRFs) regulate post-transcriptional gene expression via AGO-dependent mechanism in IL-1β stimulated chondrocytes.

J A Green, M Y Ansari, H C Ball, T M Haqqi

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Osteoarthritis and cartilage, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

58 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. The Roles of tRNA-Derived Fragments in Cancer: Updates and Perspectives.International journal of molecular sciences · 2025
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  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

4 authors at 1 institution in 1 country.

J A GreenDepartment of Anatomy and Neurobiology, Northeast Ohio Medical University, Rootstown, OH, 44272, USA.
M Y AnsariDepartment of Anatomy and Neurobiology, Northeast Ohio Medical University, Rootstown, OH, 44272, USA.
H C BallDepartment of Anatomy and Neurobiology, Northeast Ohio Medical University, Rootstown, OH, 44272, USA.
T M HaqqiDepartment of Anatomy and Neurobiology, Northeast Ohio Medical University, Rootstown, OH, 44272, USA. Electronic address: thaqqi@neomed.edu.
Northeast Ohio Medical University · US

Funding

Uridylation of miRNAs by ZCCHC6 Regulates IL-6 Expression in ArthritisR01AR067056 · NIAMS · NORTHEAST OHIO MEDICAL UNIVERSITY · PI HAQQI, TARIQ M · 2015 to 2019
$2.9M
Suppression of SHH Expression in Arthritis by Butea monospermaR01AT007373 · NCCIH · NORTHEAST OHIO MEDICAL UNIVERSITY · PI HAQQI, TARIQ M · 2013 to 2017
$2.5M
NCCIH NIH HHS R01 AT007373NIAMS NIH HHS R01 AR067056
6 · The paper itself

Abstract

objectivesRecent studies have shown that tRNA-derived RNA fragments (tRFs) are novel regulators of post-transcriptional gene expression. However, the expression profiles and their role in post-transcriptional gene regulation in chondrocytes is unknown. Here, we determined tRFs expression profile and explored tRF-3003a role in post-transcriptional gene regulation in IL-1β stimulated chondrocytes.

methodsWe used qPCR arrays to determine tRNAs and tRFs expression in age- and sex-matched primary human OA chondrocytes and TC28/I2 cells stimulated with IL-1β. Chondrocytes were transfected with tRNA-Cys

resultsIL-1β increased the expression levels of specific tRNAs and of tRF-3003a, a type 3 tRF produced by the cleavage of tRNA-Cys

conclusionsWe demonstrate that under pathological conditions chondrocytes display perturbations in the expression profile of specific tRNAs and tRFs. Furthermore, a specific tRF namely tRF-3003a can post-transcriptionally regulate JAK3 expression via AGO/RISC formation in chondrocytes. Identification of this novel mechanism may be of value in the design of precision therapies for OA.

Indexed as

Gene Expression Regulation3' Untranslated RegionsArgonaute ProteinsCell LineChondrocytesHumansInterleukin-1betaJanus Kinase 3OsteoarthritisPrimary Cell CultureRNA, MessengerRNA, Small UntranslatedRNA, TransferRNA, Transfer, Cys3' Untranslated RegionsArgonaute ProteinsInterleukin-1betaJAK3 protein, humanJanus Kinase 3RNA, MessengerRNA, Small UntranslatedRNA, TransferRNA, Transfer, CysChondrocyteJAK3Noncoding RNAOsteoarthritisTransfer RNAtRNA-derived fragments

Identifiers

PMID32407895
PMCPMC8418333
OpenAlexW3024300365

What OpenQuestion holds

Textmetadata
LicenceTDM
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.