RNA-seq of triple cultures of neurons, astrocytes and microglia treated with blood clot conditioned media, lipopolysaccharide, and Nrf2-activating drug CDDO-TFEA.
Secondary injury causes death and dependence after spontaneous intracerebral haemorrhage (ICH). We found that myelomononuclear Nrf2 is active and protective after ICH in mice. To investigate the roles of myelomononuclear Nrf2 in modulating cell autonomous and non-cell autonomous responses to the oxidative and inflammatory consequences of ICH we developed an in vitro system of co-cultures of primary mouse microglia, human astrocytes and rat neurons and performed RNA-seq, subsequently performing in-silico separation of read data into separate species, and thus separate cell types. Cultures were treated with blood clot condition media (CCM), lipopolysaccharide (LPS), and Nrf2-activating drug CDDO-TFEA, and experiments were performed using wild-type mouse microglia, and microglia from mice with global Nrf2 deletion.