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Hsa-miR-203 inhibits fracture healing via targeting PBOV1.

AbstractOBJECTIVE:
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.
AuthorsS-Y Zhang, F Gao, C-G Peng, C-J Zheng, M-F Wu
JournalEuropean 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
PMID30280758 (Publication Type: Journal Article)
Chemical References
  • MIRN203 microRNA, human
  • MicroRNAs
  • Neoplasm Proteins
  • PBOV1 protein, human
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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