Figure 7.

Graphics summarizes the roles of BOP1 knockdown in regulation of neointimal hyperplasia. Downregulating BOP1 by lentivirus, on the one hand, leads to the accumulation of free RPL11 in cytoplasm, and then RPL11 combines with MDM2, which restrains MDM2-mediated degeneration of p53, subsequently inducing p53-mediated cell cycle arrest and apoptosis; on the other hand, BOP1 knockdown impairs rRNA maturation and ribosome biogenesis and deregulates the rate of nascent proteins synthesis, thereby inhibiting neointimal hyperplasia. BOP1: blocking of proliferation 1; RPL11: ribosomal protein L11; MDM2: murine double minute 2; VSMCs: vascular smooth muscle cells.