Hsa-miR-203 inhibits fracture healing via targeting PBOV1
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.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2018 |
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| Erschienen: |
2018 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:22 |
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| Enthalten in: |
European review for medical and pharmacological sciences - 22(2018), 18 vom: 17. Sept., Seite 5797-5803 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Zhang, S-Y [VerfasserIn] |
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| Links: |
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| Themen: |
Journal Article |
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| Anmerkungen: |
Date Completed 14.11.2019 Date Revised 14.11.2019 published: Print Citation Status MEDLINE |
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| doi: |
10.26355/eurrev_201809_15905 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM289163064 |
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| 245 | 1 | 0 | |a Hsa-miR-203 inhibits fracture healing via targeting PBOV1 |
| 264 | 1 | |c 2018 | |
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| 500 | |a Date Completed 14.11.2019 | ||
| 500 | |a Date Revised 14.11.2019 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a OBJECTIVE: To explore the role of hsa-miR-203 in fracture healing and its underlying mechanism | ||
| 520 | |a 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 | ||
| 520 | |a 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 | ||
| 520 | |a CONCLUSIONS: Hsa-miR-203 inhibits fracture healing by regulating osteoblast viability and apoptosis via targeting PBOV1 | ||
| 650 | 4 | |a Journal Article | |
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| 700 | 1 | |a Peng, C-G |e verfasserin |4 aut | |
| 700 | 1 | |a Zheng, C-J |e verfasserin |4 aut | |
| 700 | 1 | |a Wu, M-F |e verfasserin |4 aut | |
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