CDC42 inhibitors regulate genes involved in skin vasculaization
RhoJ protein has 55% homology with CDC42 and is highly expressed in endothelial cells. Both proteins regulate migration and contraction in endothelial cells through the activation of typrosine kinase receptors that control angiogenesis. To better understand how CDC42 inhibitors modulate angiogenesis, we performed bulk RNA sequening on wildtype skin treated with 12 mg/kg ARN22089 or vehicle twice a day for a week. Expression profiling showed that CDC42 inhibitors modulate skin vascularization. Some of the genes downregulated after CDC42 inhibitor treatment in wildtype skin involves CDC42 signaling and cell adhesion and putative angiogenesis regulators including CD177, CCL12, and CD34. Endothelial markers such as Lyve1 and Cd34 were also downregulated. Overall design: RNA-seq profiling of wildtype (WT) mouse skin and WT skin from WT mouse treated with 12 mg/kg of ARN22089 twice a day for one week.