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Published on: August 16, 2018
Hsa-miR-203 inhibits fracture healing via targeting PBOV1
1Department of Orthopedics, The Second Hospital of Jilin University, Changchun, China. wuminfei999@163.com.
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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