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. 2016 Nov 28;8(12):3298–3310. doi: 10.18632/aging.101118

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.

Figure 3

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.