Microarray analysis of the in vivo response ofmicroglia to Aβ peptides in mice with conditional deletion of the prostaglandin EP2 receptor

Amyloid-beta (A beta) peptides accumulate in the brains of patients with Alzheimer's disease (AD), where they generate a persistent inflammatory response from microglia, the innate immune cells of the brain. The immune modulatory cyclooxygenase/prostaglandin E2 (COX/PGE(2)) pathway has been implicated in preclinical AD development, both in human epidemiology studies and in transgenic rodent models of AD [2,3]. PGE(2) signals through four G-protein-coupled receptors, including the EP2 receptor that has been investigated for its role in mediating the inflammatory and phagocytic responses to A beta [4]. To identify transcriptional differences in microglia lacking the EP2 receptor, we examined mice with EP2 conditionally deleted in Cd11b-expressing immune cells. We injected A beta peptides or saline vehicle into the brains of adult mice, isolated primary microglia, and analyzed RNA expression by microarray. The resulting datasets were analyzed in two studies [5,6], one describing the basal status of microglia with or without EP2 deletion, and the second study analyzing the microglial response to A beta. Here we describe in detail the experimental design and data analyses. The raw data from these studies are deposited in GEO, accession GSE57181 (http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE57181). (C) 2015 The Authors. Published by Elsevier Inc.