Aliskiren Improved the Endothelial Repair Capacity of Endothelial Progenitor Cells from Patients with Hypertension via the Tie2/PI3k/Akt/eNOS Signalling Pathway

Figure 6

Tie2/PI3k/AKT signalling pathway blockade inhibits the in vitro function and in vivo reendothelialization capacity of EPCs treated with aliskiren. (a–c) Quantification analysis of aliskiren-mediated migration ( vs. non-aliskiren-treated EPCs from normotensive subjects, n = 18 per group; vs. aliskiren-treated EPCs from hypertensive patients, n = 18 per group) (a), adhesion ( vs. non-aliskiren-treated EPCs from normotensive subjects, n = 18 per group; vs. aliskiren-treated EPCs from hypertensive patients, n = 18 per group) (b), and proliferation ( vs. non-aliskiren-treated EPCs from normotensive subjects, n = 18 per group; vs. aliskiren-treated EPCs from hypertensive patients, n = 18 per group) (c) of EPCs with Tie2 knockdown or after PI3k or eNOS inhibition. hpf = high-power field. (d) Quantification analysis of the aliskiren-mediated reendothelialization capacity of EPCs with Tie2 knockdown or after PI3k or eNOS inhibition ( vs. non-aliskiren-treated EPCs from normotensive subjects, n = 18 per group; vs. aliskiren-treated EPCs from hypertensive patients, n = 18 per group).

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