PU.1 dictates β-amyloid-induced TREM2 expression upregulation in microglia in a transgenic model of Alzheimer's disease.

ABSTRACT:

Introduction

Microglial dysfunction is characteristic of Alzheimer's disease (AD), with triggering receptor expressed on myeloid cells 2 (TREM2) and transcription factor PU.1 playing crucial roles. However, the relationship between TREM2 and PU.1 remains unclear.

Methods

We investigated TREM2 and PU.1 expression patterns in the 5×FAD mouse AD model. Experimental approaches included quantitative PCR, western blotting, immunofluorescence staining, chromatin immunoprecipitation, and luciferase reporter assays to examine the interaction between PU.1 and TREM2. The phagocytic function of microglial cells was evaluated using Aβ42 and Nile red fluorescent microsphere phagocytosis assays.

Results

TREM2 and PU.1 expression significantly correlated with brain β-amyloid (β) depo

SUBMITTER: Wei Z 

PROVIDER: S-EPMC12078285 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature