Related Experiment Video
Updated: Oct 21, 2025
A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures
Published on: March 18, 2021
miR-106b-5p upregulation is associated with microglial activation and inflammation in the mouse hippocampus following
Tao Yu1, Hui Fu1,2, Jing-Jing Sun1
1Department of Pediatrics, Shengjing Hospital of China Medical University, China Medical University, No. 36, Sanhao Street, Heping District, Shenyang City, 110004, Liaoning Province, China.
Abstract:
To investigate the association of miR-106b-5p with neuroinflammation and microglial activation in a status epilepticus (SE) mouse model. We examined changes in the expression of microRNA-106b-5p (miRNA-106b-5p), repulsive guidance molecule A (RGMa), triggering receptor expressed on myeloid cells 2 (TREM2), and the microglia-related markers interleukin (IL)-1β, IL-4, IL-6, IL-10, inducible nitric oxide synthase (iNOS), and arginase-1 (Arg-1) in the mouse hippocampus of the lithium-pilocarpine-induced SE mouse model. Eighty-four female C57BL/6 mice were randomly divided into a normal control group (n = 12), and six SE groups (n = 12/group), which were monitored at 6 h and at 1, 3, 7, 14, and 21 days (d) post-SE induction. Unlike in the dentate gyrus, immunohistochemical staining revealed prominent neuronal swelling at 6 h, significant neuronal loss and apoptosis on day 3, and recovery by day 14 in the hippocampal cornu ammonis (CA)1 and CA3 pyramidal cells in SE mice. We noted elevated levels of miRNA-106b-5p and all microglia-related markers, which peaked at 3 days post-SE, except IL-4, which peaked at 7 days post-SE, indicating inflammation and microglial activation. RGMa and TREM2 levels decreased at 6 h post-SE. All markers but miRNA-106b-5p, RGMa, and TREM2 returned to baseline levels at 21 days post-SE. Dual luciferase reporter gene assay showed that microRNA-106b-5p can interact with RGMa. We observed that miR-106b-5p level increased while both RGMa and TREM2 levels decreased post-SE and showed associations with microglial activation and inflammation in the mouse hippocampus, suggesting their potential as SE therapeutic targets.
Insights
MicroRNA-106b-5p and microglial markers increase during status epilepticus (SE) in mice, suggesting potential therapeutic targets. RGMa and TREM2 levels decrease post-SE, with miR-106b-5p interacting with RGMa.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- Status epilepticus (SE) is a neurological emergency characterized by prolonged seizures.
- Neuroinflammation and microglial activation are key pathological processes in SE.
- The role of specific microRNAs, like miR-106b-5p, in SE-induced neuroinflammation remains underexplored.
Purpose of the Study:
- To investigate the association of miR-106b-5p with neuroinflammation and microglial activation in a mouse model of SE.
- To examine the expression patterns of miR-106b-5p, RGMa, TREM2, and key inflammatory markers post-SE.
- To explore the potential interaction between miR-106b-5p and RGMa.
Main Methods:
- Lithium-pilocarpine-induced status epilepticus model in female C57BL/6 mice.
- Assessment of neuronal damage via immunohistochemistry at various time points post-SE.
- Quantification of miRNA-106b-5p, RGMa, TREM2, and microglia-related markers (IL-1β, IL-4, IL-6, IL-10, iNOS, Arg-1) using molecular assays.
- Dual luciferase reporter gene assay to confirm direct interaction between miR-106b-5p and RGMa.
Main Results:
- SE induced neuronal swelling, loss, and apoptosis in the hippocampus, with recovery by day 14.
- Levels of miR-106b-5p and most microglia-related markers (IL-1β, IL-6, IL-10, iNOS, Arg-1) peaked at 3 days post-SE, indicating inflammation and microglial activation.
- RGMa and TREM2 levels decreased early post-SE (6 hours), while IL-4 peaked later (7 days).
- miR-106b-5p demonstrated a direct interaction with RGMa.
- Most markers returned to baseline by 21 days, except for miR-106b-5p, RGMa, and TREM2.
Conclusions:
- miR-106b-5p levels are elevated post-SE and associated with neuroinflammation and microglial activation.
- Decreased RGMa and TREM2 levels correlate with SE-induced inflammation.
- The miR-106b-5p/RGMa axis may play a role in SE pathogenesis.
- These findings suggest miR-106b-5p, RGMa, and TREM2 as potential therapeutic targets for SE.
More Related Videos
09:07Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins
Published on: August 15, 2017
10:40Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain
Published on: October 27, 2019