Evidence map›Paper›PMID 33546582›Full record

ArticleMolecular medicine (Cambridge, Mass.)2021

Long non-coding RNA CIR inhibits chondrogenic differentiation of mesenchymal stem cells by epigenetically suppressing ATOH8 via methyltransferase EZH2.

Feng Liu, De-Ye Song, Jun Huang, Hong-Qi Yang, Di You, Jiang-Dong Ni

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

Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.3field-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

26 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. The Crucial Role of Epigenetic Modifications in Wharton's Jelly Stem Cells.International journal of molecular sciences · 2025
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  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.

Feng LiuDepartment of Orthopedics, The Second Xiangya Hospital of Central South University, No.139 Renminzhong Road, Changsha, 410011, Hunan, People's Republic of China.
De-Ye SongDepartment of Orthopedics, The Second Xiangya Hospital of Central South University, No.139 Renminzhong Road, Changsha, 410011, Hunan, People's Republic of China.
Jun HuangDepartment of Orthopedics, The Second Xiangya Hospital of Central South University, No.139 Renminzhong Road, Changsha, 410011, Hunan, People's Republic of China.
Hong-Qi YangDepartment of Orthopedics, The Third Hospital of Changsha, Changsha, 410015, Hunan, People's Republic of China.
Di YouDepartment of Orthopedics, The Second Xiangya Hospital of Central South University, No.139 Renminzhong Road, Changsha, 410011, Hunan, People's Republic of China.
Jiang-Dong NiDepartment of Orthopedics, The Second Xiangya Hospital of Central South University, No.139 Renminzhong Road, Changsha, 410011, Hunan, People's Republic of China. nijiangdong@csu.deu.cn.ORCID 0000-0001-5245-722X
Central South University · CNThird Hospital of Changsha · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOsteoarthritis (OA) is the most common articular disorder, leading to joint malfunction and disability. Although the incidence of OA is increasing globally, the treatment of OA is very limited. LncRNA CIR has been implicated in OA through unclear mechanisms. Here, we investigated the role of lncRNA CIR in chondrogenic differentiation.

methodsHuman umbilical-cord-derived mesenchymal stem cells (hUC-MSCs) were obtained from human umbilical cords. Flow cytometry was used to analyze the surface markers of hUC-MSCs. Various culture conditions and corresponding staining assays were employed to assess the differentiation abilities of hUC-MSC. qRT-PCR, western blot, and immunostaining were used to measure expression levels of related genes and proteins such as lncRNA CIR, ATOH8, EZH2, and H3K27me3. RNA immunoprecipitation assay, biotin pull-down, and chromatin immunoprecipitaion assay were performed to analyze the interactions of lncRNA CIR, EZH2, H3K27me3 and ATOH8 promoter.

resultshUC-MSCs exhibited MSCs features and could differentiate into chondrocytes under specific conditions. LncRNA CIR was downregulated while ATOH8 was upregulated during the chondrogenic differentiation of hUC-MSCs. Knockdown lncRNA CIR or overexpression of ATOH8 promoted chondrogenic differentiation. Further, lncRNA CIR bound to EZH2 and repressed ATOH8 expression via EZH2-mediated H3K27me3, which promotes the methylation of ATOH8. Inhibition of ATOH8 reversed the effects of knockdown lncRNA CIR on chondrogenic differentiation.

conclusionLncRNA CIR suppresses chondrogenic differentiation of hUC-MSCs. Mechanistically, lncRNA CIR could inhibit ATOH8 expression that functions to promote chondrogenic differentiation through EZH2-mediated epigenetic modifications.

Indexed as

AdultBasic Helix-Loop-Helix ProteinsCell DifferentiationCells, CulturedChondrocytesChondrogenesisDNA MethylationEnhancer of Zeste Homolog 2 ProteinEpigenesis, GeneticFemaleHistonesHumansMesenchymal Stem CellsPregnancyPromoter Regions, GeneticRNA, Long NoncodingATOH8 protein, humanBasic Helix-Loop-Helix ProteinsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistoneslong noncoding RNA CIR, humanRNA, Long NoncodingATOH8Chondrogenic differentiationEZH2hUC-MSCLncRNA CIROsteoarthritis

Identifiers

PMID33546582
PMCPMC7866678
OpenAlexW3128077896

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.