查看文章

Background— Prostacyclin (PGI₂) and thromboxane (TxA₂) effect disparate outcomes for atherogenesis and the response to vascular injury; PGI₂, a vasodilator and inhibitor of platelet aggregation, limits the deleterious actions of TxA₂, a vasoconstrictor and platelet activator. Dimerization of their G protein-coupled receptors, IP and TP, evokes a modified cellular response through which IP/TP counter-balance may be effected. We examined the consequence of IP/TP interaction for the regulatory pathways of both receptors.

Methods and Results— TPα overexpressed in HEK293 cells or expressed endogenously in aortic smooth muscle cells (ASMCs) was internalized after selective activation of either TP or IP. Homologous trafficking of TP was unaltered by coexpression of IP. Heterologous sequestration of TPα required the physical presence of activated IP, in transfected and native cells, but was independent of IP …