NOGOB Receptor Deficiency Increases Cerebrovascular Permeability and Hemorrhage

Cerebral cavernous malformation (CCM) lesions are caused by loss of function of CCM genes. Previous study showed that NOGOB receptor (NGBR) knockout in endothelial cells results in cerebrovascular lesions in the mouse embryo. However, the molecular mechanism by which NGBR regulates CCM1/2 expression has not been explained. To determine the molecular mechanism, RNA sequencing analysis was used to examine changes in the transcriptome in human brain microvascular endothelial cells (HBMVECs). Validated small interfering RNA was used to knockdown NGBR in HBMVECs. Then, isolated RNA was used to examine the alteration of transcriptomic profiling using RNA sequencing. The results indicate that NGBR-mediated histone acetylation is a potential target for preventing the onset and progression of sporadic CCM.