Home General Physiology and Biophysics 2025 General Physiology and Biophysics Vol.44, No.1, p, 81–92, 2025

Journal info


Founded: 1982
ISSN 1338-4325 (online)
ISSN 0231-5882 (print)
Published in English,
6 times per year

Aims and Scope
Editorial Info
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.
Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

General Physiology and Biophysics Vol.44, No.1, p, 81–92, 2025

Title: Transcription factor Yy1 modulates Trem1 to control LPS-triggered neuroinflammation and oxidative stress in mouse astrocytes via the NF-κB pathway
Author: Wei Ke, Zhuofan Ye, Yiyun Huang, Shineng Ye
Abstract:  Dysfunction of astrocytes has a crucial role in the pathology of depression. Here, we aimed to define the exact action of the ubiquitous transcription factor (TF) Yin Yang-1 (Yy1) in depression pathogenesis and astrocytic dysfunction. A chronic unpredictable mild stress (CUMS) mouse model was generated. Primary mouse astrocytes were exposed to lipopolysaccharide (LPS). Cell growth was determined by CCK-8 and EdU assays. The direct interaction of Yy1 and the Trem1 promoter was validated by chromatin immunoprecipitation (ChIP) and luciferase assays. In CUMS mice, the levels of Yy1 and inflammatory cytokines were augmented and oxidative stress was enhanced. Functionally, disruption of Yy1 or triggering receptor expressed on myeloid cell 1 (Trem1) relieved LPS-triggered pro-growth, pro-inflammation, and pro-oxidative stress effects in mouse astrocytes. Mechanistically, Yy1 directly promoted the transcription and expression of Trem1 by binding to the Trem1 promoter. Yy1 disruption exerted regulatory impacts in LPS-induced mouse astrocytes via down-regulation of Trem1. Additionally, the Yy1/Trem1 cascade could modulate the activation of the NF-κB signaling in mouse astrocytes. Our study defines that Yy1 disruption relieves LPS-triggered neuroinflammation and oxidative stress in mouse astrocytes via the NF-κB pathway by down-regulating Trem1, providing possible strategies for depression treatment.
Keywords: Astrocytes — Depression — Transcription factor Yy1 — Trem1 — Neuroinflammation — Oxidative stress
Year: 2025, Volume: 44, Issue: 1 Page From: 81, Page To: 92
doi:10.4149/gpb_2024037


download file


© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.