The role of antimiR-26a-5p/biphasic calcium phosphate in repairing rat femoral defects.
Yuan X., Han L., Lin H., Guo Z., Huang Y., Li S.
Animal Study, published in Int J Mol Med (2019) — summary generated from the PubMed abstract.
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
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
- Int J Mol Med (2019)
- Country
- Greece
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 31257525
- PMCID
- PMC6658005
- DOI
- 10.3892/ijmm.2019.4249
- Citations
- 6
Abstract (original English)
Although miRNAs have been implicated in the osteogenic differentiation of stem cells, their role in bone repair and reconstruction in tissue‑engineered bone grafts remains unclear. We previously reported that microRNA (miR)‑26a‑5p inhibited the osteogenic differentiation of adipose‑derived mesenchymal stem cells (ADSCs), and that antimiR‑26a‑5p exerted the opposite effect. In the present study, the role of miR‑26a‑5p‑ and antimiR‑26a‑5p‑modified ADSCs combined with biphasic calcium phosphate (BCP) scaffolds was evaluated in a rat femur defect model. The aim of the present study was to improve the understanding of the role of miR‑26a‑5p in bone regeneration in vivo, as well as to provide a new method to optimize the osteogenic ability of BCPs. ADSCs were infected with Lv‑miR‑26a‑5p, Lv‑miR‑NC, Lv‑antimiR‑26a‑5p or Lv‑antimiR‑NC respectively, and then combined with BCP scaffolds to repair rat femoral defects. Using X‑rays, micro‑computed tomography and histology at 2, 4, and 8 weeks postoperatively, the quantity and rate of bone regeneration were analyzed, revealing that they were the highest in animals treated with antimiR‑26a‑5p and the lowest in the miR‑26a‑5p treatment group. The expression levels of osteocalcin, collagen I, Runt‑related transcription factor 2, Wnt family member 5A and calmodulin‑dependent protein kinase II proteins were positively correlated with the bone fo
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.
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