Key result
Aliskiren improved the in vitro migration, proliferation, and adhesion, and in vivo reendothelialization capability of endothelial progenitor cells from hypertensive patients via the Tie2 pathway.
Why the study?
The mechanism underlying the favourable effect of aliskiren on endothelial progenitor cells (EPCs) from patients with hypertension was unclear.
Does aliskiren pretreatment improve the endothelial repair capacity of endothelial progenitor cells from patients with hypertension?
Does aliskiren pretreatment improve the endothelial repair capacity of endothelial progenitor cells from patients with hypertension?
Aliskiren enhances the endothelial repair capacity of EPCs from hypertensive patients through the Tie2/PI3k/Akt/eNOS signaling pathway, suggesting potential benefits in hypertension-related vascular injury.
May inform endothelial repair therapies in hypertension; leaves open clinical translation from animal data.
BACKGROUND: Studies show that aliskiren exerts favourable effects not only on endothelial progenitor cells (EPCs) but also on endothelial function. However, the mechanism of the favourable effect of aliskiren on EPCs from patients with hypertension is unclear and remains to be further studied. METHODS: The object of this study was to investigate and assess the in vitro function of EPCs pretreated with aliskiren. After treated with aliskiren, the human EPCs were transplanted into a nude mouse model of carotid artery injury, and the in vivo reendothelialization of injured artery was estimated by staining denuded areas with Evans blue dye via tail vein injection. RESULTS: We found that aliskiren increased the in vitro migration, proliferation, and adhesion of EPCs from patients with hypertension in a dose-dependent manner and improved the reendothelialization capability of these EPCs. Furthermore, aliskiren increased the phosphorylation of Tie2, Akt, and eNOS. After the blockade of the Tie2 signalling pathway, the favourable effects of aliskiren on the in vitro function and in vivo reendothelialization capability of EPCs were suppressed. CONCLUSIONS: This study demonstrates that aliskiren can improve the in vitro function and in vivo reendothelialization capability of EPCs from patients with hypertension via the activation of the Tie2/PI3k/Akt/eNOS signalling pathway. These findings further indicate that aliskiren is an effective pharmacological treatment for cell-based repair in hypertension-related vascular injury.
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Yao et al. (2020) studied Hypertension. Aliskiren was evaluated on In vitro migration, proliferation, and adhesion of EPCs, and in vivo reendothelialization capability. Aliskiren improved the in vitro migration, proliferation, and adhesion, and in vivo reendothelialization capability of endothelial progenitor cells from hypertensive patients via the Tie2 pathway.
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