Evidence map›Paper›PMID 26969024›Full record

ArticleCell proliferation2016

MicroRNA-30a promotes extracellular matrix degradation in articular cartilage via downregulation of Sox9.

Tingjie Chang, Jie Xie, Hongzhuo Li, Dong Li, Ping Liu, Yihe Hu

Open access · bronzeAbstract read
In one paragraph

Article in Cell proliferation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
6.6field-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

21 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. MiR-30 Family: A Novel Avenue for Treating Bone and Joint Diseases?International journal of medical sciences · 2023
    Review
  6. Article
  7. Article
  8. Crosstalk Among circRNA/lncRNA, miRNA, and mRNA in Osteoarthritis.Frontiers in cell and developmental biology · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Role of MicroRNA in Osteoarthritis.Journal of arthritis · 2017
    Article
  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

6 authors at 3 institutions in 1 country.

Tingjie ChangDepartment of Orthopedics, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.
Jie XieDepartment of Orthopedics, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.
Hongzhuo LiDepartment of Orthopedics, Peace Hospital of Changzhi Medical College, Changzhi, Shanxi, 046000, China.
Dong LiDepartment of Orthopedics, Peace Hospital of Changzhi Medical College, Changzhi, Shanxi, 046000, China.
Ping LiuDepartment of Orthopedics, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.
Yihe HuDepartment of Orthopedics, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.
Changzhi Medical College Peace Hospital · CNXiangya Hospital Central South University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesSox9 has recently been reported to be a key mediator during cartilage degradation in osteoarthritis (OA). Our aim was to clarify the role of microRNA-30a (miR-30a) and its target gene Sox9 in regulation of extracellular matrix (ECM) degradation in OA. MATERIALS AND

methodsExpression of miR-30a in cartilage tissues and in primary chondrocytes from healthy and OA donors, was determined by real-time PCR, and levels of Sox9 mRNA and protein were analyzed by real-time PCR and western blotting, respectively. Subsequently, the target of miR-30a was predicted by bioinformatics and confirmed using a luciferase assay. Expression of ECM-related genes was determined by tissue-specific staining, immunofluorescence, real-time PCR, and western blotting. The role of miR-30a in OA was examined in vivo using a collagenase-induced OA rat model.

resultsmiR-30a was significantly upregulated and Sox9 was downregulated in primary chondrocytes from cartilage taken from OA donors compared to healthy controls. We showed that miR-30a specifically bound to the 3' UTR of Sox9, and overexpression of miR-30a downregulated expression levels of Sox9, proteoglycan aggrecan, and Col II compared to those induced by small interfering RNA transfection to knockdown Sox9. miR-30a inhibition reversed the effects of ECM degradation in vitro and in vivo.

conclusionsmiR-30a acts as a virulence MRA in OA, promoting ECM degradation by targeting Sox9 and by modulating activity of its downstream effectors Col II and proteoglycan aggrecan.

Indexed as

AdultAgedAggrecansAnimalsCartilage, ArticularCells, CulturedChondrocytesCollagenDisease Models, AnimalDown-RegulationExtracellular MatrixFemaleHumansInterleukin-1betaMaleMicroRNAsAggrecansCollagenIL1B protein, humanInterleukin-1betaMicroRNAsMIRN30b microRNA, humanMIRN30 microRNA, ratRNA, MessengerRNA, Small InterferingSOX9 protein, humanSOX9 Transcription Factor

Identifiers

PMID26969024
PMCPMC6496402
OpenAlexW2296380648

What OpenQuestion holds

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Read underepoch 390

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.