Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMC

Over-expression of MEG3 promotes differentiation of bone marrow mesenchymal stem cells into chondrocytes by regulating miR-129-5p/RUNX1 axis

Zhu J., Fu Q., Shao J., Peng J., Qian Q., Zhou Y.

Animal Study on Cartilage Damage, published in Cell Cycle (2021) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Cell Cycle (2021)
Reported sample size
—
Source database
Europe PMC
PMID
33410373
PMCID
PMC7849720
DOI
10.1080/15384101.2020.1863043
Citations
9

Abstract (original English)

This study explored the role of MEG3 in the cartilage differentiation of bone marrow mesenchymal stem cells (BMSCs). We investigated the effects of over-expression and knockdown of MEG3 on cell viability, cell differentiation, and the expressions of MEG3, miR-129-5p, COL2, chondrocyte differentiation-related genes (sry-type high-mobility-group box 9 (SOX9), SOX5, Aggrecan, silent information regulator 1 (SIRT1), and Cartilage oligomeric matrix protein (COMP)). The targeting relationship between MEG3 and miR-129-5p and the target gene of miR-129-5p was confirmed through Starbase, TargetScan and luciferase experiments. Finally, a series of rescue experiments were conducted to study the regulatory effects of MEG3 and miR-129-5p. BMSCs were identified as CD29 + and CD44 + positive, and their differentiation was time-dependent. As BMSCs differentiated, MEG3 expression was up-regulated, but miR-129-5p was down-regulated. Over-expressed MEG3 promoted the viability and differentiation of BMSCs, up-regulated the expressions of COL2 and chondrocyte differentiation-related genes, and inhibited miR-129-5p. Runt-related transcription factor 1 (RUNX1) was negatively regulated as a target gene of miR-129-5p. Results of rescue experiments showed that the inhibitory effect of miR-129-5p mimic on BMSCs could be partially reversed by MEG3. Over-expression of MEG3 regulated the miR-129-5p/RUNX1 ax

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
Cells, CulturedChondrocytesMesenchymal Stem CellsBone MarrowAnimalsRatsRats, Sprague-DawleyMicroRNAsCell DifferentiationCell Survival

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