Research Paper Volume 8, Issue 12 pp 3298—3310

miR-34a is a common link in both HIV- and antiretroviral therapy-induced vascular aging

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Figure 4. Both antiretroviral agents and HIV-Tat transgene have the enhanced vascular aging, which could be inhibited by miR-34a knockdown in mice in vivo. HIV-1 transgenic mice have enhanced vascular aging as shown by the impaired endothelial function (A) and the reduced telomerase activity (B). Mice with antiretroviral therapy have the enhanced vascular aging as shown by the impaired endothelial function (C) and the reduced telomerase activity (D). The expression of miR-34a in mouse arteries was successfully down-regulated by AntagomiR-34a (40 mg/kg, iv per week, via tail vein) in vivo (E). Compared with that from vehicle treated mice, mice with antiretroviral therapy had the enhanced vascular aging as shown by the impaired endothelial function (F) and the decreased telomerase activity (G), which was inhibited via miR-34a knockdown. Compared with that from vehicle treated mice, vascular aging was significantly inhibited via miR-34a knockdown in HIV-1 Tat transgenic mice (H and I). Note: n=6-8; *p<0.05 compared with control groups.