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Updated: Jan 23, 2026

Acute and Chronic Tactile Sensory Testing after Spinal Cord Injury in Rats
Published on: April 4, 2012
MiR-137-5p alleviates inflammation by upregulating IL-10R1 expression in rats with spinal cord injury
1Department of Spine Surgery, Luoyang Orthopedic Hospital of Henan Province, Zhengzhou, China. 305360418@qq.com.
Objective:
This study aims to explore the potential functions of miR-137-5p and interleukin-10R1 (IL-10R1) in mediating the immune inflammation after spinal cord injury (SCI).
Materials And Methods:
Firstly, primary microglia were isolated from the spinal cord of newborn rats. Expression levels of miR-137-5p and IL-10R1 in LPS-induced microglia were determined by quantitative Real-time polymerase chain reaction (qRT-PCR). In addition, mRNA expressions of Janus kinase (Jak1) and signal transducer and activator of transcription 3 (STAT3) were also examined by qRT-PCR. SCI model in rats was established and randomly assigned to three different groups: Sham group, SCI group and miR-137-5p mimic group. Within one week of spinal injury, relative levels of miR-137-5p and IL-10R1 in rats of different groups were detected by qRT-PCR. The mRNA levels of JAK1, tyrosine kinase (Tyk2) and STAT3 in rats were also measured. Moreover, protein expression of IL-1β, TNF-α and IL-6 in rats was measured by Western blotting. Finally, the improvement of locomotor function in three groups of rats within 4 weeks via BBB rating scale.
Results:
Transfection of miR-137-5p mimics upregulated relative levels of IL-10R1, JAK1 and STAT3 in in vitro cultured microglia. Similarly, IL-10R1/JAK1/STAT3 pathway was activated in rats administrated with miR-137-5p mimics. Nevertheless, relative levels of classical inflammatory stimulators IL-1β, TNF-α and IL-6 were downregulated accordingly by miR-137-5p overexpression. Moreover, miR-137-5p effectively improved the locomotor function of rats after SCI.
Conclusions:
MiR-137-5p exerts an anti-inflammatory response by upregulating IL-10R1, thus improving locomotor function and alleviating spinal cord injury.
Insights
MicroRNA-137-5p (miR-137-5p) enhances spinal cord injury recovery by upregulating interleukin-10 receptor 1 (IL-10R1), reducing inflammation, and improving motor function.
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Spinal cord injury (SCI) triggers significant immune inflammation, leading to secondary damage and functional deficits.
- MicroRNAs (miRNAs) play crucial roles in regulating cellular responses, including inflammation, following SCI.
- Identifying specific miRNAs and their targets involved in SCI pathogenesis is essential for developing therapeutic strategies.
Purpose of the Study:
- To investigate the functional role of miR-137-5p in the inflammatory response post-SCI.
- To elucidate the relationship between miR-137-5p and interleukin-10 receptor 1 (IL-10R1) in SCI.
- To assess the impact of miR-137-5p modulation on locomotor recovery after SCI.
Main Methods:
- Primary rat microglia were cultured and stimulated to assess miR-137-5p and IL-10R1 expression via qRT-PCR.
- A rat SCI model was established, with groups receiving sham surgery, SCI, or miR-137-5p mimics.
- Expression of miR-137-5p, IL-10R1, JAK1, STAT3, and inflammatory cytokines (IL-1β, TNF-α, IL-6) was quantified.
- Locomotor function was evaluated using the BBB rating scale.
Main Results:
- Overexpression of miR-137-5p upregulated IL-10R1, JAK1, and STAT3 in microglia and in vivo.
- The IL-10R1/JAK1/STAT3 signaling pathway was activated by miR-137-5p mimics.
- miR-137-5p overexpression significantly reduced the expression of pro-inflammatory cytokines IL-1β, TNF-α, and IL-6.
- Administration of miR-137-5p mimics improved locomotor function in rats following SCI.
Conclusions:
- MiR-137-5p functions as an anti-inflammatory agent in the context of spinal cord injury.
- Upregulation of IL-10R1 by miR-137-5p is a key mechanism mediating its protective effects.
- Modulating miR-137-5p offers a promising therapeutic avenue for alleviating SCI and promoting functional recovery.
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