Expression of OATP2B1 as determinant of drug effects in the microcompartment of the coronary artery.

摘要: Clinical success of coronary drug-eluting stents (DES) is hampered by simultaneous reduction smooth muscle cell (HCASMC) and endothelial proliferation due to unspecific cytotoxicity currently used compounds. Previous in vitro data showing SMC-specific inhibition suggested that statins may be suitable candidates for DES. It was aim this study further investigate as DES drug identify mechanisms contributing their cell-selectivity. In assays comparing the influence various on HCASMC cells confirmed atorvastatin exhibits HCASMC-specificity. Due similar expression levels target HMG-CoA reductase both types, cellular accumulation assessed, revealing enhanced uptake most likely driven significant OATP2B1, a known transporter atorvastatin. accordance with finding endogenous OATP2B1 influenced we tool teniposide new candidate HCASMC-specific effects. We describe determinant pharmacokinetics artery. Indeed, endogenously expressed significantly influences substrate drugs, thereby governing specificity. Screening drugs interaction promote SMC-specificity.