miR‑10a‑5p inhibits osteogenic differentiation of bone marrow‑derived mesenchymal stem cells

Abstract

The use of human bone marrow mesenchymal stem cells (hBMScs) as a tissue engineering application for individuals affected by osteoporosis and other types of bone loss diseases has been well studied in recent years. The osteogenic differentiation of hBMScs can be regulated by a number of cues. Micrornas (mirnas/mirs) serve as the key regulators of various biological processes; however, to the best of our knowledge, no information exists with regards to the specific modulatory effects of mir-10a-5p on osteogenic differentiation of hBMScs. The aim of the present study was to investigate the relationship between hBMScs and mir-10a-5p and, ultimately, to determine how mir-10a-5p affects the osteogenic differentiation process of hBMScs in vitro and in vivo. The hBMScs used in the present study were transfected with mirVana™ mirna inhibitors and mimics, and transfection efficiency was assessed by fluorescence microscopy and reverse transcription-quantitative Pcr (rT-qPcr). Viability of hBMScs following transfection was analyzed using a cell counting Kit-8 assay. The mrna expression levels of specific osteoblast markers, including alkaline phosphatase (alP) and runt-related transcription factor 2 (runX2) were measured using rT-qPcr and western blot analysis. new bone formation was evaluated by Goldner's trichrome staining and micro-cT analysis in vivo. No significant difference in cell viability was observed among the different groups 24 h post-transfection. overexpression of mir-10a-5p inhibited the expression of osteoblast makers in hBMScs, whereas inhibition of mir-10a-5p upregulated the expression of alP and runX2 in vitro. Furthermore, mir-10a-5p acted as a suppressor during the process of new bone formation in vivo. In conclusion, the findings of the present study suggested that mir-10a-5p served as a negative regulatory factor during osteoblast differentiation of hBMScs and may be utilized in a treatment approach for bone repair in osteogenic-related diseases.

LncPVT1 regulates osteogenic differentiation of human periodontal ligament cells via miR‐10a‐5p/brain‐derived neurotrophic factor

“…Bioinformatics analysis suggested that lncPVT1 promoted the osteoblast differentiation of PDLCs by binding to miR‐10a‐5p, which is involved in cell proliferation, 38 apoptosis, 39 and the progression of osteoarthritis and cancers 40,41 . A previous study showed that miR‐10a‐5p could inhibit the osteogenic differentiation of bone mesenchymal stem cells (BMSCs) 42 . Here, we revealed the binding potential of lncPVT1 and miR‐10a‐5p using the RIP assay.…”

“…40,41 A previous study showed that miR-10a-5p could inhibit the osteogenic differentiation of bone mesenchymal stem cells (BMSCs). 42 Here, we revealed the binding potential of lncPVT1 and miR-10a-5p using the RIP assay. Besides, miR-10a-5p was significantly downregulated during osteogenesis and negatively correlated with the expression level of lncPVT1.…”

miRNA-10a-5p Targeting the BCL6 Gene Regulates Proliferation, Differentiation and Apoptosis of Chicken Myoblasts

“…In vitro experiments, miRNA-10a-5p played a negative regulatory role in the osteogenic differentiation of human bone marrow MSCs by targeting ALP and RUNX2 genes. Similarly, in vivo miRNA-10a-5p negatively regulated the osteogenic differentiation of human bone marrow mesenchymal stem cells [ 30 ]. In our study, the effect of miRNA-10a-5p on chicken myoblasts’ differentiation was similar to that described above.…”

Therapeutic Potential of Exosomes Derived from Adipose Tissue-Sourced Mesenchymal Stem Cells in the Treatment of Neural and Retinal Diseases

“…As determined by transcriptome and multi-omics sequencing technologies, AT-MSC-Exos are enriched with bioactive molecules (microRNAs (miRNAs), enzymes, cytokines, chemokines, immunoregulatory, trophic, and growth factors), that are responsible for AT-MSC-Exo-dependent beneficial effects in inflamed and injured neural and retinal tissues (Table 1) [20][21][22][23][24][25][26][27].…”