IQGAP1 causes choroidal neovascularization by sustaining VEGFR2-mediated Rac1 activation.

ABSTRACT: Loss of visual acuity in neovascular age-related macular degeneration (nAMD) occurs when factors activate choroidal endothelial cells (CECs) to transmigrate the retinal pigment epithelium into the sensory retina and develop into choroidal neovascularization (CNV). Active Rac1 (Rac1GTP) is required for CEC migration and is induced by different AMD-related stresses, including vascular endothelial growth factor (VEGF). Besides its role in pathologic events, Rac1 also plays a role in physiologic functions. Therefore, we were interested in a method to inhibit pathologic activation of Rac1. We addressed the hypothesis that IQGAP1, a scaffold protein with a Rac1 binding domain, regulates pathologic Rac1GTP in CEC migration and CNV. Compared to littermate Iqgap1^+/+, Iqgap1^-/-

SUBMITTER: Wang H 

PROVIDER: S-EPMC7530064 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature