TIE2 links MEKK3–KLF2/4 and PI3K signaling in cerebral cavernous malformation
Lun Li·Mark L. Kahn·Hiroki Hongo·Jian Ren·Robert Shenkar·Rashad Jabarkheel·Siqi Gao·Sweta Narayan·Maxwell Frankfurter·Alan T. Tang·Jisheng Yang·Mei Chen·Jenna Bockman·Patricia Mericko-Ishizuka·Roberto Alcazar·Georgio Sader·Javed Iqbal·Serena Kinkade·Rhonda Lightle·Andrew K. Ressler·Xianghu Qu·H. Scott Baldwin·Douglas A. Marchuk·Issam A. Awad·Jan-Karl Burkhardt·Michael Potente·Marco Castro
Cerebral cavernous malformations (CCMs) are vascular lesions in the central nervous system that can cause strokes and seizures. Aggressive CCM growth follows an endothelial cell two-hit mechanism in which enhanced MEKK3-KLF2/4 signaling stimulates PI3K signaling, but how these pathways are linked has been undefined. Here, we use human CCM specimens, two mouse models of CCM disease, and primary human endothelial cells to examine the roles of the major endothelial growth factor receptors, VEGFR2 a
