Project description:Cerebral cavernous malformation (CCM) immunothrombosis is the connection between immune cells, platelet activation, coagulation cascades and astrocyte-CCM endothelium interaction, and its excessive activation may contribute to neurological disabilities in CCM disease. We characterized the spatial organization of CCM immunothrombosis observed in Pdcd10BECKObrains under normoxic conditions using the murine 10X Genomics Visium Spatial Gene Expression platform.
Project description: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. However, the role of active drivers of angiogenesis as CCM disease modifiers in human disease remains unclear. To examine if hypoxia, a driver of angiogenesis, may contribute to CCM exacerbation, we performed bulk RNA-seq of brain tissue from P50 Pdcd10BECKO mice under normoxia and hypoxia. P50 Pdcd10fl/fl littermate controls under normoxia and hypoxia were used as controls.