Related Experiment Video
Updated: Aug 19, 2026
A Chronic Immobilization Stress Protocol for Inducing Depression-Like Behavior in Mice
Published on: May 15, 2019
TREM2 regulates BV2 microglia activation and influences corticosterone-induced neuroinflammation in depressive
Jingjing Shi1, Xiaohong Wang1, Chuanyi Kang1
1Department of Psychiatry, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, Heilongjiang Province 150001, China.
Abstract:
Depressive disorders is a serious mental illness, and its underlying pathological mechanisms remain unclear. The overactivation of microglia and neuroinflammation are thought to play an essential role in the occurrence and development of depressive disorders. TREM2, an immune protein mainly expressed in microglia, is an important part of nerve cells involved in inflammatory response. Corticosterone (CORT) is often referred to as a stress hormone and plays a role in the immune system and stress response. Therefore, this study investigated the role of TREM2 in CORT-induced BV2 cell damage and preliminarily analyzed the effects of TREM2 on JAK2/STAT3 signaling pathway and microglia polarization. The cell model of CORT-induced depression in vitro was established, and the effect of CORT on the activity of BV2 microglia was detected by CCK8. Plasmid transfection was used to overexpress and interfere with TREM2 in BV2 cells cultured by CORT. Western blotting, PCR, and ELISA analyzed the expression of related proteins and inflammatory factors. The results showed that CORT could affect BV2 cell proliferation and TREM2 levels. In the presence of CORT, overexpression of TREM2 decreased the levels of TNF-α, IL-1β, and IL-6 and increased the levels of IL-10. Interference with TREM2 increased the levels of TNF-α, IL-1β, and IL-6 and decreased the levels of IL-10. TREM2 can affect the release of inflammatory factors through the JAK2/STAT3 signaling pathway and regulate the M1/M2 phenotypic transformation of microglia. TREM2 plays a role in regulating CORT-induced inflammatory responses, revealing the influence of TREM2 on the neuroinflammatory pathogenesis of depressive disorders and suggesting that TREM2 may be a new target for the prevention and treatment of depressive disorders.
Insights
TREM2 protein modulates neuroinflammation in a depression model. Upregulating TREM2 reduces inflammatory factors and may offer a new therapeutic target for depressive disorders.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Depressive disorders involve neuroinflammation and microglial overactivation.
- TREM2, an immune protein in microglia, influences inflammatory responses.
- Corticosterone (CORT) is a stress hormone impacting the immune system.
Purpose of the Study:
- Investigate TREM2's role in CORT-induced BV2 cell damage.
- Analyze TREM2's effects on the JAK2/STAT3 pathway and microglia polarization.
- Explore TREM2 as a potential therapeutic target for depression.
Main Methods:
- Established a cell model of CORT-induced depression in vitro.
- Utilized CCK8 assay to assess CORT's effect on BV2 cell activity.
- Employed plasmid transfection for TREM2 overexpression and interference.
- Analyzed protein and inflammatory factor expression via Western blotting, PCR, and ELISA.
Main Results:
- CORT affected BV2 cell proliferation and TREM2 levels.
- TREM2 overexpression reduced TNF-α, IL-1β, IL-6, and increased IL-10.
- TREM2 interference increased TNF-α, IL-1β, IL-6, and decreased IL-10.
- TREM2 influenced inflammatory factor release via the JAK2/STAT3 pathway and regulated microglia polarization.
Conclusions:
- TREM2 plays a critical role in regulating CORT-induced inflammatory responses.
- TREM2 influences the neuroinflammatory pathogenesis of depressive disorders.
- TREM2 presents a potential novel therapeutic target for depressive disorders.
