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Inhibition of long non-coding RNA TSIX accelerates tibia fraction healing via binding and positively regulating the
1Department of Orthopedics Trauma, Trauma Center, Shanghai General Hospital of Nanjing Medical University, Shanghai, China. wangqiugen@yahoo.com.
Objective:
Fragile fracture patients need to be treated with long-term fixation and the recovery process is slow. Several studies have shown that the fracture healing process is related to gene expression. We aimed to investigate the role of long chain non-coding RNA TSIX (lncRNA TSIX) on fracture healing after tibial fracture (TF) and explore the molecular mechanism underlying its action.
Materials And Methods:
The male C57BL/6J mice were used to construct TF models and osteoblasts were used as in vitro model. The proliferation, apoptosis, and osteogenesis-related genes of Col1a1, Col-II, and Col-X were detected to evaluate the role of lncRNA TSIX in vivo and in vitro after TF. Haematoxylin-eosin (HE) staining was conducted to confirm the fracture healing conditions.
Results:
We found that LncRNA TSIX expression in plasma of TF mice significantly upregulated in a time-dependent manner. Overexpression of lncRNA TSIX could significantly inhibit proliferation but promote apoptosis and regulate the osteogenesis-related genes expression by binding and positively regulate sex-determining region Y box 6 (SOX6) expression, while knockdown of lncRNA TSIX showed the opposite effect in osteoblastic cells. Inhibition of lncRNA TSIX could improve fracture healing after TF.
Conclusions:
Taken together, our study supported that knockdown of lncRNA TSIX could promote the tibia fracture healing by binding and inhibiting the SOX6 expression. We suggest that lncRNA TSIX/SOX may be the potential targets for the treatment of TF.
Insights
Knocking down long chain non-coding RNA TSIX (lncRNA TSIX) promotes tibia fracture healing by inhibiting SOX6 expression. This suggests lncRNA TSIX/SOX6 may be a therapeutic target for fracture treatment.
Area of Science:
- Molecular Biology
- Genetics
- Orthopedics
Background:
- Fracture healing is a complex process influenced by gene expression.
- Long chain non-coding RNAs (lncRNAs) are increasingly recognized for their roles in biological processes.
- Tibial fractures (TF) require long-term treatment and have a slow recovery.
Purpose of the Study:
- To investigate the role of lncRNA TSIX in tibial fracture healing.
- To explore the molecular mechanism of lncRNA TSIX in fracture repair.
- To identify potential therapeutic targets for TF.
Main Methods:
- Tibial fracture models were established in male C57BL/6J mice.
- Osteoblast cell cultures were used as an in vitro model.
- Expression of lncRNA TSIX and osteogenesis-related genes (Col1a1, Col-II, Col-X) was analyzed.
- Proliferation and apoptosis were assessed.
- Hematoxylin-eosin (HE) staining was performed to evaluate fracture healing.
Main Results:
- lncRNA TSIX expression was upregulated in plasma of TF mice in a time-dependent manner.
- Overexpression of lncRNA TSIX inhibited osteoblast proliferation and promoted apoptosis.
- lncRNA TSIX positively regulated SOX6 expression, affecting osteogenesis-related genes.
- Knockdown of lncRNA TSIX improved fracture healing in vivo and in vitro.
Conclusions:
- lncRNA TSIX knockdown promotes tibia fracture healing by inhibiting SOX6 expression.
- The lncRNA TSIX/SOX6 axis is a potential therapeutic target for tibial fracture treatment.
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