Evidence map›Paper›PMID 32248331›Full record

ArticleInflammation2020

The Fibroblast-Like Synoviocyte Derived Exosomal Long Non-coding RNA H19 Alleviates Osteoarthritis Progression Through the miR-106b-5p/TIMP2 Axis.

Fengjin Tan, Dongbo Wang, Zhongkai Yuan

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

65 citing papers in PubMed, 91 citations in OpenAlex.

  1. Review
  2. Article
  3. From pathogenesis to therapy: extracellular vesicles in osteoarthritis.Frontiers in bioengineering and biotechnology · 2026
    Review
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  15. Review
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  17. Exosomes in cartilage microenvironment regulation and cartilage repair.Frontiers in cell and developmental biology · 2025
    Review
  18. Review
  19. Article
  20. Review

5 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

3 authors at 1 institution in 1 country.

Fengjin Tan *Orthopedics and Traumatology, Yantai Hospital of Traditional Chinese Medicine, 39, Happy Road, Yantai City, 264000, China. tanfjyhtcm@sina.com.
Dongbo Wang *Orthopedics and Traumatology, Yantai Hospital of Traditional Chinese Medicine, 39, Happy Road, Yantai City, 264000, China.
Zhongkai YuanMedical imaging Department, Yantai Hospital of Traditional Chinese Medicine, 39, Happy Road, Yantai City, 264000, China.
Yantaishan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) is a common degenerative joint disease that affects people worldwide. The interaction between fibroblast-like synoviocytes (FLSs) and chondrocytes may play a vital role in OA disease pathology. However, the underlying mechanisms by which FLSs exert regulatory effects on chondrocytes still need to be elucidated. Exosomes, small membrane vesicles secreted from living cells, are known to play a variety of roles in mediating cell-to-cell communication through the transferring of biological components such as non-coding RNAs and proteins. Here, we investigate the cellular processes of chondrocytes regulated by FLS-derived exosomes and the mechanisms of action underlying the functions of exosomes in OA pathogenesis. We observed that exosome-mediated cartilage repair was characterized by increased cell viability and migration as well as alleviated matrix degradation. Using chondrocyte cultures, the enhanced cellular proliferation and migration during exosome-mediated cartilage repair was linked to the exosomal lncRNA H19-mediated regulation of the miR-106b-5p/TIMP2 axis. Transfection of miR-106-5p mimics in chondrocytes significantly decreased cell proliferation and migration, promoted matrix degradation characterized by elevated MMP13 and ADAMTS5 expression, and reduced the expression of COL2A1 and ACAN in chondrocytes. Furthermore, we found that TIMP2 was directly regulated by miR-106-5p. Co-transfections of miR-106-5p mimics and TIMP2 resulted in higher levels of COL2A1 and ACAN, but lower levels of MMP13 and ADAMTS5. Together, these observations demonstrated that the lncRNA H19 may promote chondrocyte proliferation and migration and inhibit matrix degradation in OA possibly by targeting the miR-106b-5p/TIMP2 axis. In the future, H19 may serve as a potential therapeutic target for the treatment of OA.

Indexed as

AdolescentAdultAgedAnimalsCells, CulturedDisease ProgressionExosomesFemaleFibroblastsHumansMaleMicroRNAsMiddle AgedOsteoarthritisRats, Sprague-DawleyRNA, Long NoncodingH19 long non-coding RNAMicroRNAsMIRN106 microRNA, humanRNA, Long NoncodingTIMP2 protein, humanTissue Inhibitor of Metalloproteinase-2ChondrocytesExosomesLncRNA H19miR-106b-5pOsteoarthritis

Identifiers

PMID32248331
OpenAlexW3015080700

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.