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Author Spotlight: Insight Into Innovations in Spinal Cord Injury Research
Published on: January 19, 2024
MicroRNA-185 regulates spinal cord injuries induced by thoracolumbar spine compression fractures by targeting
Pengfei Zhao1, Shaochun Wang1, Yingjie Zhou1
1Luoyang Orthopedic-Traumatological Hospital, Luoyang, Henan 471002, P.R. China.
Abstract:
The aims of the present study were to examine the expression of transforming growth factor (TGF)-β1 and microRNA (miR)-185 in the bone tissue, blood and cerebrospinal fluid of patients with spinal cord injuries and to evaluate the regulation of spinal cord injuries by miR-185. A total of 44 patients with spinal cord injuries induced by thoracolumbar spine compression fractures, who were hospitalized at Luoyang Orthopedic-Traumatological Hospital between June 2012 and February 2015 were enrolled in the present study. Among the patients enrolled, 18 underwent surgery between 1 and 7 days following fracture, and 26 patients underwent surgery between 8 and 14 days following fracture. Bone tissue, peripheral blood and cerebrospinal fluid were subsequently harvested from patients for analysis. Reverse transcription-quantitative polymerase chain reaction was performed to determine the expression of miR-185 and TGF-β1 mRNA. Western blotting was performed to evaluate TGF-β1 protein expression in bone tissue and ELISA was employed to quantify TGF-β1 protein expression in the blood and cerebrospinal fluid. TGF-β1 mRNA and protein levels in bone tissue, blood and cerebrospinal fluid from patients who underwent surgery 8-14 days post-fracture were significantly higher than those who underwent surgery 1-7 days post-fracture (P<0.05). By contrast, miR-185 levels were significantly lower in bone tissue, blood and cerebrospinal fluid from patients who underwent surgery 8-14 days post-fracture compared with those who underwent surgery 1-7 days post-fracture (P<0.05). The results of the present study desmonstrate that the upregulation of TGF-β1 in the bone tissue, blood and cerebrospinal fluid of patients with spinal cord injuries induced by thoracolumbar spine compression fractures is correlated with the downregulation of miR-185. Furthermore, miR-185 may target TGF-β1, affecting its transcription and translation, indicating that it serves an important role in spinal cord injuries induced by thoracolumbar spine compression fractures.
Insights
In spinal cord injuries, higher transforming growth factor-beta 1 (TGF-β1) levels correlate with lower microRNA-185 (miR-185) levels. This suggests miR-185 plays a role in regulating TGF-β1 in these injuries.
Area of Science:
- Orthopedics
- Molecular Biology
- Neuroscience
Background:
- Spinal cord injuries (SCIs) resulting from thoracolumbar spine compression fractures present complex challenges.
- Understanding the molecular mechanisms, including growth factors and microRNAs, is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the expression of transforming growth factor-beta 1 (TGF-β1) and microRNA-185 (miR-185) in patients with SCIs.
- To explore the regulatory role of miR-185 in the context of SCIs.
Main Methods:
- Analysis of bone tissue, blood, and cerebrospinal fluid from 44 SCI patients.
- Quantification of miR-185 and TGF-β1 mRNA using reverse transcription-quantitative polymerase chain reaction (RT-qPCR).
- Assessment of TGF-β1 protein levels via Western blotting and ELISA.
Main Results:
- Significantly higher TGF-β1 mRNA and protein levels were observed in patients undergoing surgery 8-14 days post-fracture compared to those operated on within 1-7 days.
- Conversely, miR-185 levels were significantly lower in the later surgery group (8-14 days).
- A strong inverse correlation was found between TGF-β1 upregulation and miR-185 downregulation in SCI patients.
Conclusions:
- The findings indicate that miR-185 may target TGF-β1, influencing its transcription and translation.
- miR-185 plays a significant role in the pathophysiology of SCIs induced by thoracolumbar spine compression fractures.
- This study highlights a potential molecular pathway for therapeutic intervention in SCIs.
