BioProject

Previous studies from our laboratory using mice with macrophage-specific loss of Trpc3 function revealed a significant, selective effect of Trpc3 in the biology of M1, or inflammatory macrophages. More...

Previous studies from our laboratory using mice with macrophage-specific loss of Trpc3 function revealed a significant, selective effect of Trpc3 in the biology of M1, or inflammatory macrophages. Whereas the activation of some components of the unfolded protein response and the pro-apoptotic mediators CAMKII and STAT1 was found impaired in the Trpc3-deficient M1 cells, gathering insight on all of the molecular signatures within macrophages that might be affected by Trpc3 requires more than a simple query for known candidate molecules. In the present study we conducted RNA-seq analysis to interrogate the transcriptome of M1 macrophages derived from mice with macrophage-specific loss of TRPC3 function and their littermate controls. Gene ontology analysis revealed enrichment in a majority of processes associated to cellular movement and lipid signaling, whereas the enriched KEGG pathways included networks for calcium signaling, cell adhesion molecules, cell cycle and focal adhesion, and salivary secretion, among others. This is the first deep transcriptomic analysis of macrophages in the context of TRPC3 deficiency and the data presented thus constitutes a unique resource for further exploring novel functions of TRPC3 in macrophage biology. Overall design: RNA sequencing of bone marrow derived M1 macrophages from control and Trpc3-deficient mice RNA samples in triplicate, using Illumina. Less...