Is glial cell-induced endothelial morphogenesis inhibited by interfering with extracellular signal-regulated kinase signaling?
The mechanism underlying activation of ERK is involved in reorganization of the actin cytoskeleton, and induction of VEGF and MMP-9, thereby stimulating endothelial cell morphogenesis. These studies clearly provide experimental evidence that ERK inhibition diminishes glial-induced endothelial-cell morphogenesis; therefore, interfering with ERK signaling may be a viable approach to target angiogenesis.
Routine specimens for blood culture may not be needed from patients hospitalized with acute PID.