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MiR-126 ameliorates neuropathic pain through suppression of macrophage migration and inflammatory response by targeting EFhd2
Abstract
Purpose: To study the molecular mechanism of miR-126 in partial sciatic nerve ligation-induced neuropathic pain.
Methods: Mice were divided into four groups: sham, partial sciatic nerve ligation (PSL), PSL+miRnegative control (NC) agomir, and PSL+miR-126 agomir. Tactile allodynia and thermal hyperalgesia were tested to evaluate the effect of PSL surgery and miR-126 overexpression on mice in each group. Expression levels of TNF-α, IL-6, and IL-1β were tested by enzyme-linked immunoassay to verify the anti-inflammatory effects of PSL surgery and miR-126 overexpression. Immunofluorescence staining was applied to investigate macrophage number, whereas quantitative PCR was applied to investigate miR-126 expression levels in each group. J774A.1 macrophage migration was evaluated by Transwell assays after administration of lipopolysaccharide (LPS) and transfection with miR-126 mimics and NC mimics, respectively. Finally, bioinformatics methods and dual-luciferase reporter assays were applied together to ascertain the interaction between miR-126 and EFhd2.
Results: MiR-126 expression was downregulated in the sciatic nerve of neuropathic pain model mice, and miR-126 overexpression alleviated neuropathic pain symptoms. Overexpression of miR-126 inhibited the inflammatory response and migration of macrophages in mice. miR-126 targets and regulates EFhd2 expression level.
Conclusion: MiR-126 suppresses macrophage inflammatory response and migration, and ameliorates PSL-induced neuropathic pain in mice by targeting EFhd2.
