mRNA expression changes in CCM3-deficient endothelial cells

Loss-of-function variants in CCM3/PDCD10 predispose to cerebral cavernous malformations (CCMs) that are vascular lesion of the central nervous system. Using CRISPR/Cas9 genome editing and RNA sequencing, we have shown that long-term inactivation of CCM3 in human endothelial cells dysregulates fibronectin expression and thus impairs the assembly of a functional fibronectin matrix by endothelial cells. Overall design: Examination of the mRNA expression profile of 3 wild-type CI-huVEC lines and 3 clonal CCM3-knockout CI-huVEC lines.