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Updated: Nov 25, 2025

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
Published on: July 3, 2020
MiR-19b-3p accelerates bone loss after spinal cord injury by suppressing osteogenesis via regulating PTEN/Akt/mTOR
1Department of Orthopedics, Shengjing Hospital of China Medical University, Shenyang, People's Republic of China.
Abstract:
Rapid and extensive bone loss, one of the skeletal complications after spinal cord injury (SCI) occurrence, drastically sacrifices the life quality of SCI patients. It has been demonstrated that microRNA (miRNA) dysfunction plays an important role in the initiation and development of bone loss post-SCI. Nevertheless, the effect of miR-19b-3p on bone loss after SCI is unknown and the accurate mechanism is left to be elucidated. The present work was conducted to explore the role of miR-19b-3p/phosphatase and tensin homolog deleted on chromosome ten (PTEN) axis on osteogenesis after SCI and further investigates the underlying mechanisms. We found that miR-19b-3p level was increased in the femurs of SCI rats with decreased autophagy. The overexpression of miR-19b-3p in bone marrow mesenchymal stem cells (BMSCs) targeted down-regulation of PTEN expression, facilitated protein kinase B (Akt) and mammalian target of rapamycin (mTOR) phosphorylation, and thereby suppressing BMSCs osteogenic differentiation via autophagy. Besides, the inhibiting effects of miR-19b-3p on osteogenic differentiation of BMSCs could be diminished by autophagy inducer rapamycin. Meanwhile, bone loss after SCI in rats was also reversed by antagomir-19b-3p treatment, suggesting miR-19b-3p was an essential target for osteogenic differentiation via regulating autophagy. These results indicated that miR-19b-3p was involved in bone loss after SCI by inhibiting osteogenesis via PTEN/Akt/mTOR signalling pathway.
Insights
MicroRNA-19b-3p exacerbates bone loss after spinal cord injury (SCI) by inhibiting osteogenesis. Targeting miR-19b-3p with antagomirs can reverse this bone loss, offering a potential therapeutic strategy.
Area of Science:
- Biomedical research
- Molecular biology
- Skeletal biology
Background:
- Spinal cord injury (SCI) leads to significant bone loss, impacting patient quality of life.
- MicroRNA (miRNA) dysfunction is implicated in post-SCI bone loss, but specific mechanisms remain unclear.
- The role of miR-19b-3p in SCI-induced bone loss requires elucidation.
Purpose of the Study:
- To investigate the role of the miR-19b-3p/PTEN axis in osteogenesis following SCI.
- To explore the underlying molecular mechanisms, including autophagy and signaling pathways.
Main Methods:
- Analysis of miR-19b-3p levels in SCI rat femurs.
- Overexpression of miR-19b-3p in bone marrow mesenchymal stem cells (BMSCs).
- Investigation of PTEN, Akt, and mTOR phosphorylation.
- Assessment of autophagy modulation using rapamycin.
- Treatment of SCI rats with antagomir-19b-3p.
Main Results:
- miR-19b-3p levels were elevated in SCI rat femurs with reduced autophagy.
- Overexpressing miR-19b-3p in BMSCs suppressed osteogenic differentiation by downregulating PTEN and activating Akt/mTOR signaling.
- Autophagy inhibition was linked to miR-19b-3p's suppressive effect on osteogenesis.
- Rapamycin treatment mitigated the inhibitory effects of miR-19b-3p.
- Antagomir-19b-3p administration reversed bone loss in SCI rats.
Conclusions:
- miR-19b-3p promotes bone loss post-SCI by inhibiting osteogenesis.
- The miR-19b-3p/PTEN/Akt/mTOR pathway regulates osteogenic differentiation via autophagy.
- miR-19b-3p is a potential therapeutic target for treating bone loss after SCI.
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