Abstract | OBJECTIVE: To explore the role of hsa-miR-203 in fracture healing and its underlying mechanism. PATIENTS AND METHODS: Expression levels of hsa-miR-203 and PBOV1 in patients with hand fractures and intra-articular fractures after treatment were detected by quantitative Real-Time-Polymerase Chain Reaction (qRT-PCR). Viability and apoptosis of osteoblast cell line hFOB1.19 after hsa-miR-203 overexpression or knockdown were detected by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The target gene of hsa-miR-203 was predicted by bioinformatics and verified by dual- luciferase reporter gene assay. Rescue experiments were conducted to further verify whether hsa-miR-203 could participate in fracture healing via PBOV1. RESULTS: No significant hsa-miR-203 expression was found in patients with hand fractures and intra-articular fractures after treatment for 7 days, which was remarkably upregulated on the 14th day. PBOV1 expression was gradually downregulated as treatment time prolongation. Overexpression of hsa-miR-203 decreased cell viability, but induced apoptosis of hFOB1.19 cells. Bioinformatics predicted that PBOV1 might be the target gene of hsa-miR-203, which was further verified by dual- luciferase reporter gene assay. The effect of hsa-miR-203 on viability and apoptosis of hFOB1.19 cells was reversed after the PBOV1 knockdown. CONCLUSIONS:
Hsa-miR-203 inhibits fracture healing by regulating osteoblast viability and apoptosis via targeting PBOV1.
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Authors | S-Y Zhang, F Gao, C-G Peng, C-J Zheng, M-F Wu |
Journal | European review for medical and pharmacological sciences
(Eur Rev Med Pharmacol Sci)
Vol. 22
Issue 18
Pg. 5797-5803
(09 2018)
ISSN: 2284-0729 [Electronic] Italy |
PMID | 30280758
(Publication Type: Journal Article)
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Chemical References |
- MIRN203 microRNA, human
- MicroRNAs
- Neoplasm Proteins
- PBOV1 protein, human
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Topics |
- Apoptosis
(physiology)
- Cell Proliferation
(physiology)
- Cell Survival
(physiology)
- Cells, Cultured
- Down-Regulation
- Fracture Healing
(physiology)
- Humans
- MicroRNAs
(biosynthesis, blood, physiology)
- Neoplasm Proteins
(biosynthesis, blood)
- Osteoblasts
(metabolism, physiology)
- Time Factors
- Up-Regulation
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