Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

The role of miR-31-modified adipose tissue-derived stem cells in repairing rat critical-sized calvarial defects.

Deng Y., Zhou H., Zou D., Xie Q., Bi X., Gu P.

Animal Study on Chronic Wound, published in Biomaterials (2013) — 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
Biomaterials (2013)
Country
Netherlands
Reported sample size
—
Source database
PubMed
PMID
23768901
DOI
10.1016/j.biomaterials.2013.05.042
Citations
97

Abstract (original English)

With the increasing application of microRNAs (miRNAs) in the treatment and monitoring of different diseases, miRNAs have become an important tool in biological and medical research. Recent studies have proven that miRNAs are involved in the osteogenic differentiation of stem cells. However, few studies have reported the use of miRNA-modified adult stem cells to repair critical-sized defects (CSDs) using tissue engineering technology. It is known that miR-31 is a pleiotropically acting miRNA that inhibits cancer metastasis and targets special AT-rich sequence-binding protein 2 (Satb2) in fibroblasts. However, it is not clear whether the function of miR-31 is to enhance adipose tissue-derived stem cell (ASC) osteogenesis, along with its association with Satb2, during osteogenic differentiation and bone regeneration. In this study, we systematically evaluated the function of miR-31 in enhancing ASC osteogenesis and the therapeutic potential of miR-31-modified ASCs in a rat CSD model with β-tricalcium phosphate (β-TCP) scaffolds. ASCs were treated with lentivirus (Lenti)-miR-31, Lenti-as-miR-31 (antisense) or Lenti-NC (negative control). These genetically modified ASCs were then combined with β-TCP scaffolds to repair CSDs in rats. The results showed that in cultured ASCs in vitro, Lenti-as-miR-31 significantly enhanced osteogenic mRNA and protein expression when compared with the

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
Adipose TissueAnimalsBlotting, NorthernBlotting, WesternCell LineElectrophoretic Mobility Shift AssayMaleMicroRNAsRatsReal-Time Polymerase Chain Reaction

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