GSE160092
The cannabinoid agonist WIN55,212-2 (WIN) suppresses the inflammation-associated transcriptional response of astrocytes to interleukin 1 beta
Accumulating evidence suggest that the endocannabinoid system is an attractive target to attenuate inflammatory responses that are implicated in neurodegeneration. Alterations in astrocytic functions play a crucial role in neuroinflammation as a consequence of the loss of their neuroprotective role or the gain of their toxic inflammatory properties. In this study, we explore the possible immunosuppressive action of the cannabinoid receptor agonist WIN55,212-2 using an in vitro model of primary human astrocytes that are activated by the pro-inflammatory cytokine interleukin 1 beta (IL1B). Genome-wide transcriptomic analysis using RNA-seq revealed that the pretreatment of astrocytic cultures with WIN55, 212-2 prevents the transcriptional activation of pro-inflammatory genes induced by IL1B. We report the immunosuppressive function of WIN55,212-2 in replicates RNA samples that were extracted from human astrocyte cultures established from one donor. Overall design: primary astrocytes cultures were collected from two biological replicates and RNA samples were analyzed by RNA-seq for each of 4 conditions (Vehicle, IL1B 6hr, WIN 24hr, WIN 24hr + IL1B 6hr)