Evidence map›Paper›PMID 31571401›Full record

ArticleJournal of cellular and molecular medicine2019

LncRNA PART-1 targets TGFBR2/Smad3 to regulate cell viability and apoptosis of chondrocytes via acting as miR-590-3p sponge in osteoarthritis.

Chao Lu, Zheng Li, Shouye Hu, Yuanzhen Cai, Kan Peng

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Crosstalk Among circRNA/lncRNA, miRNA, and mRNA in Osteoarthritis.Frontiers in cell and developmental biology · 2021
    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

5 authors at 2 institutions in 1 country.

Chao LuDepartment of Joint Surgery, Xi'an Honghui Hospital, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Zheng LiDepartment of Emergency, the First Affiliated Hospital of Xi'an Medical University, Xi'an, China.
Shouye HuDepartment of Joint Surgery, Xi'an Honghui Hospital, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Yuanzhen CaiDepartment of Joint Surgery, Xi'an Honghui Hospital, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Kan PengDepartment of Joint Surgery, Xi'an Honghui Hospital, Xi'an Jiaotong University Health Science Center, Xi'an, China.ORCID 0000-0002-6485-4369
Xi'an Honghui Hospital · CNXi'an Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) is a degenerative joint disease that commonly occurs in the elderly. This study focused on apoptosis and explored the modulating effects of long non-coding (lncRNAs) prostate androgen-regulated transcript-1 (PART-1) on chondrocytes apoptosis. In the present study, the PART-1 expression level was down-regulated in the OA cartilages. Silence of PART-1 decreased the cell viability and promoted chondrocytes apoptosis. Overexpression of PART-1 could reverse the effects induced by interleukin 1β (IL-1β) stimulation, thus slowing down the apoptosis rate. MiR-590-3p was found to be the potential target, and RNA immunoprecipitation and luciferase activity assay confirmed the binding between PART-1 and miR-590-3p. Moreover, miR-590-3p was down-regulated by PART-1 and was negatively associated with PART-1. Transforming growth factor-beta receptor type 2 (TGFBR2) was positively associated with PART-1. Down-regulation of PART-1 decreased cell viability and induced cell apoptosis, which was partially reversed by miR-590-3p silence or TGFBR2 overexpression; while overexpression of PART-1 increased the cell viability and decreased the caspase 3 activity and apoptotic rates, and the effects were partially attenuated by miR-590-3p overexpression or silence of TGFBR2 in IL-1β-stimulated chondrocytes. Knock-down of PART-1 down-regulated both Smad3 and p-Smad3 protein levels, which was reversed by miR-590-3p inhibition or TGFBR2 overexpression. Smad3 expression level was lower in the OA group than that in the normal group and was positively associated with the PART-1 expression level. Collectively, the study revealed that lncRNA PART-1 regulates the apoptosis of chondrocytes in OA by acting as a sponge for miR-590-3p, which subsequently regulates TGFBR2/Smad3 signalling.

Indexed as

ApoptosisCell LineCell SurvivalChondrocytesGene Expression RegulationHumansMicroRNAsOsteoarthritisReceptor, Transforming Growth Factor-beta Type IIRNA InterferenceRNA, Long NoncodingRNA, UntranslatedSignal TransductionSmad3 ProteinMicroRNAsMIRN590 microRNA, humanPART-1 RNA, humanReceptor, Transforming Growth Factor-beta Type IIRNA, Long NoncodingRNA, UntranslatedSmad3 ProteinTGFBR2 protein, humanapoptosischondrocytesmiR-590-3posteoarthritisPART-1TGFBR2

Identifiers

PMID31571401
PMCPMC6850963
OpenAlexW2979126880

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.