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RBM5 and p53 expression after rat spinal cord injury: implications for neuronal apoptosis
Jinlong Zhang1, Zhiming Cui1, Guijuan Feng2
1Department of Spine Surgery, The Second Affiliated Hospital of Nantong University, Nantong University, 226001 Nantong, Jiangsu, People's Republic of China.
Abstract:
RBM5 (RNA-binding motif protein 5), a nuclear RNA binding protein, is known to trigger apoptosis and induce cell cycle arrest by regulating the activity of the tumor suppressor protein p53. However, its expression and function in spinal cord injury (SCI) are still unknown. To investigate whether RBM5 is involved in central nervous system injury and repair, we performed an acute SCI model in adult rats in this study. Our results showed RBM5 was unregulated significantly after SCI, which was accompanied with an increase in the levels of apoptotic proteins such as p53, Bax, and active caspase-3. Immunofluorescent labeling also showed that traumatic SCI induced RBM5 location changes and co-localization with active caspase-3 in neurons. To further probe the role of RBM5, a neuronal cell line PC12 was employed to establish an apoptotic model. Knockdown of RBM5 apparently decreased the level of p53 as well as active caspase-3, demonstrating its pro-apoptotic role in neurons by regulating expressions of p53 and caspase-3. Taken together, our findings indicate that RBM5 promotes neuronal apoptosis through modulating p53 signaling pathway following SCI.
Insights
RNA-binding motif protein 5 (RBM5) promotes neuronal apoptosis after spinal cord injury (SCI) by regulating the p53 signaling pathway. This study reveals RBM5
Area of Science:
- Neuroscience
- Molecular Biology
- Cellular Biology
Background:
- RNA-binding motif protein 5 (RBM5) is a nuclear protein known to regulate apoptosis and cell cycle arrest via the tumor suppressor p53.
- The role and expression of RBM5 in the context of spinal cord injury (SCI) remain largely uncharacterized.
Purpose of the Study:
- To investigate the involvement of RBM5 in central nervous system (CNS) injury and repair following acute SCI.
- To elucidate the specific function of RBM5 in neuronal apoptosis after SCI.
Main Methods:
- An acute SCI model was established in adult rats.
- Expression levels of RBM5 and apoptotic markers (p53, Bax, active caspase-3) were analyzed post-SCI.
- Immunofluorescence was used to examine RBM5 localization and co-localization with active caspase-3 in neurons.
- A PC12 neuronal cell line was utilized to create an apoptotic model for RBM5 knockdown experiments.
Main Results:
- RBM5 expression was significantly upregulated following SCI in rats.
- SCI induced increased levels of apoptotic proteins including p53, Bax, and active caspase-3.
- RBM5 showed altered localization and co-localized with active caspase-3 in neurons after traumatic SCI.
- Knockdown of RBM5 in PC12 cells reduced p53 and active caspase-3 levels, confirming its pro-apoptotic role.
Conclusions:
- RBM5 plays a significant role in promoting neuronal apoptosis after spinal cord injury.
- RBM5 modulates the p53 signaling pathway, contributing to neuronal cell death following SCI.
- These findings highlight RBM5 as a potential therapeutic target for mitigating neuronal loss in SCI.
