E-MTAB-9252
A PGE2-MEF2A axis enables context-dependent control of inflammatory gene expression
BMDMs or iMACs were generated via differentiation of bone marrow cells or immortalized precursors, respectively, in culture media containing m-CSF for 7 day. Upon differentiation, BMDMs or iMacs were left untreated or stimulated as described below. 1) BMDM WT were stimulated with LPS, PGE2, LPS+PGE2 for 4 hours: each condition in triplicate. This experiment was performed to assess chromatin accessibility in the concomitant presence of pro-inflammatory (LPS) and anti-inflammatory stimuli (PGE2). 2) MEF2A-deficient iMac clones (D7, A7, A8, C7) and MEF2A-proficient (referred to as wild-type) iMac clones (NE, B3 and D10) were generated via CRISPR/Cas9 and stimulated or not with LPS for either 4 hours: each condition in single. This experiment was performed to assess the role in MEF2a in controlling chromatin accessibility upon LPS stimulation.
BMDMs or iMACs were generated via differentiation of bone marrow cells or immortalized precursors, respectively, in culture media containing m-CSF for 7 day. Upon differentiation, BMDMs or iMacs were left untreated or stimulated as described below. 1) BMDM WT were stimulated with LPS, PGE2, LPS+PGE2 for 4 hours: each condition in triplicate. This experiment was performed to assess chromatin accessibility in the concomitant presence of pro-inflammatory (LPS) and anti-inflammatory stimuli (PGE2). 2) MEF2A-deficient iMac clones (D7, A7, A8, C7) and MEF2A-proficient (referred to as wild-type) iMac clones (NE, B3 and D10) were generated via CRISPR/Cas9 and stimulated or not with LPS for either 4 hours: each condition in single. This experiment was performed to assess the role in MEF2a in controlling chromatin accessibility upon LPS stimulation.