Brain endothelial cells with inflammatory signature in CCM disease in hypoxia and normoxia conditions

The CCM endothelium is hypersensitive to angiogenesis and can induce a hypoxic program associated with changes in angiogenesis, inflammation, and endothelial-cell metabolism under normoxic conditions. It has been suggested that environmental, genetic, or biological factors act as disease modifiers. However, the underlying mechanisms are not entirely understood. To assess whether mild hypoxia accelerates CCM, we employed a CCM mouse model (Pdcd10BECKO;Aldh1l1-EGFP/Rpl10a). Brain endothelial cells (BECs) were isolated from Slco1c1-iCreERT2;Pdcd10fl/fl;Aldh1l1-EGFP/Rpl10a mice to as previously described. BECs mRNAs were from isolated microvesels from cerebral tissue of mice age P50 exposed to hypoxia or normoxia conditions.