Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

Exosomes derived from human CD34 + stem cells transfected with miR-26a prevent glucocorticoid-induced osteonecrosis of the femoral head by promoting angiogenesis and osteogenesis

Zuo R., Kong L., Wang M., Wang W., Xu J., Chai Y.

Animal Study on Hip, published in Stem Cell Res Ther (2019) — 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
Read the A–D evidence level guide

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
Stem Cell Res Ther (2019)
Reported sample size
—
Source database
Europe PMC
PMID
31730486
PMCID
PMC6858646
DOI
10.1186/s13287-019-1426-3
Citations
77

Abstract (original English)

Background Damaged endothelial cells and downregulated osteogenic ability are two key pathogenic mechanisms of glucocorticoid (GC)-induced osteonecrosis of the femoral head (ONFH). Recent studies suggested that transplantation of CD34 + stem cell-derived exosomes (CD34 + -Exos) can treat ischemic diseases by promoting neovascularization and that miR-26a is an important positive regulator of osteogenesis. Moreover, the biological effect of exosomes is closely related to their cargo miRNAs. However, it is not clear whether increasing the abundance of miR-26a in CD34 + -Exos will inhibit the progress of GC-induced ONFH. Methods MiR-26a was overexpressed in CD34 + -Exos (miR-26a-CD34 + -Exos) to increase their osteogenic potential. The angiogenic potential of miR-26a-CD34 + -Exos was then examined through evaluations of migration and tube-forming capacities in vitro. In addition, in order to observe the osteogenic effect of miR-26a-CD34 + -Exos on bone marrow stromal cells (BMSCs), Alizarin red staining, alkaline phosphatase (ALP) activity assays, and qPCR were carried out. Finally, miR-26a-CD34 + -Exos were injected into a GC-induced ONFH rat model to prevent the progress of GC-induced ONFH. The biological effects of miR-26a-CD34 + -Exos on the ONFH model were evaluated by micro-CT, angiography, and histological staining. Results Our data showed that miR-26a-CD34 + -Exos enhanced

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
Stem CellsAnimalsHumansRats, Sprague-DawleyFemur Head NecrosisDisease Models, AnimalMicroRNAsAntigens, CD34GlucocorticoidsTransfection

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