A preliminary study on the interaction between Asn-Gly-Arg (NGR)-modified multifunctional nanoparticles and vascular epithelial cells

Liu, Chunxi; Liu, Tingxian; Yu, Xiaoyue; Gu, Yizhu

Then, MβCD was used to deplete cholesterol from the cell membrane and thereby damage caveolae, leading to the blocked internalization of TPIC. Additionally, the co-localization of TPIC and CAV1 was also inhibited after MβCD treatment. Obviously, cholesterol depletion can destroy the integrity of caveolae, affect the interaction between TPIC and CAV1 and inhibit TPIC entry into the cells. The above studies supported the important role of caveolae in TPIC entry into HUVEC. The subsequent inhibition studies also suggested that the internalization of TPIC in HUVEC was a process combining CME and CvME. The existence of CME was inferred through our above and previously reported results. Nevertheless, the dominant intracellular mechanism of TPIC entry into HUVEC was the CvME. This result was consistent with our original hypothesis.