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Updated: Dec 30, 2025
Identifying Microglia and Peripheral Infiltrating Macrophages in the Injured Spinal Cords Using Flow Cytometry
Published on: June 24, 2025
microRNA-182-5p alleviates spinal cord injury by inhibiting inflammation and apoptosis through modulating the
1Department of Acupuncture, Tuina, Traumatology, The Sixth People's Hospital Affiliated to Shanghai Jiaotong University Shanghai 200233, China.
Abstract:
Inflammatory response and apoptosis play an important role in progression of spinal cord injury (SCI). Recently, aberrant microRNAs (miRNAs) have emerged as a key regulator in SCI. However, it remains unknown whether and how miRNAs mediated the inflammatory response after SCI. The aim of this study was to evaluate the potential role of miRNAs in SCI and elucidate underlying molecular mechanisms. First, we analyzed the microRNA expression profile in spinal cords from rats following SCI, using miRNA microarray. Interestingly, miR-182-5p was one of miRNAs most significantly downregulated in SCI. It has been reported as an inflammation suppressor in different organ injury models. Here, we used a cell model to verify the regulatory function and mechanism of miR-182-5p on inflammatory response in SCI. Overexpression of miR-182-5p attenuated H2O2-induced inflammation as reflected by reduction in proinflammatory cytokines in C8-D1A cells. Meanwhile, enhanced miR-182-5p expression significantly suppressed H2O2-induced apoptosis. Toll-like receptor 4 (TLR4), an important regulator of nuclear factor kappa-B (NF-κB) signaling pathway, was identified as a novel target of miR-182-5p in C8-D1A cells. Furthermore, overexpression of TLR4 reversed inhibitory effects of miR-182-5p overexpression on inflammation and apoptosis. More importantly, we found that miR-182-5p blocked phosphorylation of nuclear p65 and promoted phosphorylation of IκB-α in H2O2-treated C8-D1A cells. Our results confirm that miR-182-5p alleviates inflammation and apoptosis via inactivation of TLR4/NF-κB pathway in an H2O2-induced cell model. Our findings suggest that miR-182-5p may be a potential therapeutic target of SCI in the future.
Insights
MicroRNA-182-5p significantly reduces inflammation and apoptosis in spinal cord injury models. This microRNA targets Toll-like receptor 4, offering potential therapeutic strategies for spinal cord injury.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Spinal cord injury (SCI) involves inflammation and apoptosis.
- MicroRNAs (miRNAs) are implicated as key regulators in SCI.
- The role of miRNAs in mediating SCI-related inflammation remains unclear.
Purpose of the Study:
- To investigate the role of miRNAs in SCI.
- To elucidate the molecular mechanisms by which miRNAs regulate inflammation and apoptosis after SCI.
- To evaluate miR-182-5p as a potential therapeutic target for SCI.
Main Methods:
- MicroRNA expression profiling in rat SCI models using miRNA microarray.
- Cellular studies using C8-D1A cells to assess miR-182-5p function in H2O2-induced inflammation and apoptosis.
- Identification of Toll-like receptor 4 (TLR4) as a direct target of miR-182-5p.
- Analysis of the TLR4/NF-κB signaling pathway.
Main Results:
- miR-182-5p was significantly downregulated in SCI.
- Overexpression of miR-182-5p reduced pro-inflammatory cytokines and apoptosis in H2O2-treated cells.
- TLR4 was identified as a direct target of miR-182-5p.
- miR-182-5p inactivated the TLR4/NF-κB pathway by blocking p65 phosphorylation and promoting IκB-α phosphorylation.
Conclusions:
- miR-182-5p alleviates inflammation and apoptosis in a cellular SCI model by inactivating the TLR4/NF-κB pathway.
- miR-182-5p demonstrates potential as a therapeutic target for spinal cord injury.
