Project description:Transcription profiles of BV2 microglial cell lines: unstimulated, stimulated with LPS or transfected with constitutively active Stat1 and Stat3.
Project description:This study employed a coculture system of BMSCs and BV2 cells , with one group receiving LPS stimulation and the other not receiving LPS stimulation, to clarify the mechanism by which bone marrow mesenchymal stem cells (BMSCs) inhibit the activation of microglia
Project description:To comprehensively study the intracellular signaling changes and explore the underlying mechanisms of baicalein-mediated microglial responses, we employed systemic proteomic approach, using target-free SWATH mass spectra (SWATH-MS), focusing on intracellular proteins. BV2 cells were treated with LPS followed by the addition of vehicle or baicalein and they were cultured for a total of 48 hours before being collected for proteomic analysis.
Project description:The OPTN gene is linked to neurodegenerative diseases like amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), which are characterized by chronic microglial activation. Optineurin regulates inflammatory signaling, autophagy, and trafficking, but its role in microglia is not well understood. We used bulk RNA sequencing to profile CRISPR-Cas9-mediated optineurin knockout (KO) and wild-type (WT) BV2 microglia under basal conditions and upon LPS stimulation. At baseline, optineurin KO altered approximately 7% of the transcriptome, with a notable downregulation of type I interferon and antiviral pathways. LPS stimulation in wild-type cells triggered a broad transcriptional shift (~35% of genes). This LPS-induced response was blunted in optineurin-deficient microglia, with ~16% of genes changed relative to the KO baseline. Furthermore, LPS-treated optineurin KO microglia notably diverged from LPS-treated wild-type cells, with ~26% differentially expressed genes. Our findings establish optineurin as a key regulator of the microglial transcriptome. Its loss weakens basal interferon-mediated immune surveillance and decouples the canonical inflammatory response from cell cycle arrest upon activation.
Project description:This study investigates the molecular mechanisms underlying the interaction between Carfilzomib (CFZ) and Herpes Simplex Virus type 1 (HSV-1) infection in microglial cells. Using the BV2 microglial cell line, we performed RNA sequencing to dissect the transcriptional responses under different conditions. Cells were either infected with HSV-1 (MOI=1) for 24 hours or left uninfected, and subsequently treated with 30 nM Carfilzomib (CFZ) or the vehicle control (DMSO) 6 hours post infection.
