Research Paper Volume 8, Issue 12 pp 3298—3310
miR-34a is a common link in both HIV- and antiretroviral therapy-induced vascular aging
Figure 3. Both antiretroviral agents and HIV-Tat protein induce senescence of ECs, which could be inhibited by miR-34a knockdown or miR-34a knockout. Antiretroviral agents ritonavir (7.5 µmol/L), or lopinavir (10 µmol/L) plus ritonavir (2 µmol/L) (lopinavir/ritonavir) could induce EC senescence as shown by the increased beta-gal staining (A and B), increased ROS production (C), decreased EC proliferation (D) and increased apoptosis induced by H2O2 (100 µM) (E and F). EC senescence was enhanced by HIV-Tat protein (100 nM) as shown by the increased beta-gal staining (G). Both antiretroviral agents (H) and HIV-Tat protein (I) induced senescence of ECs could be inhibited by miR-34a knockdown AntagomiR-34a (30 nM). The ECs from miR-34a knockout mice were resistant to antiretroviral agents (J) and HIV-Tat protein (K) induced senescence of ECs. Note: n=6; *p<0.05 compared with control groups.