Abstract
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.
Highlights
As a major cardiovascular disease, hypertension usually impairs target organs and increases the risk of cardiovascular events
Relevant studies demonstrate that the reendothelialization capability of endothelial progenitor cells (EPCs) is beneficial to maintaining the integrity of the vascular endothelium after arterial injury [8, 9], which is crucial for the prophylaxis and Cardiology Research and Practice treatment of cardiovascular disease [8, 10,11,12,13,14,15]
Recent clinical trials proved that the state of hypertension and prehypertension leads to the declined number and dysfunction of circulating EPCs, implying that this impaired endogenous endothelial repair capacity is involved in mediating hypertension-related endothelial dysfunction and vascular injury [4, 16]
Summary
As a major cardiovascular disease, hypertension usually impairs target organs and increases the risk of cardiovascular events. Studies show that aliskiren exerts favourable effects on endothelial progenitor cells (EPCs) and on endothelial function. The mechanism of the favourable effect of aliskiren on EPCs from patients with hypertension is unclear and remains to be further studied. After the blockade of the Tie signalling pathway, the favourable effects of aliskiren on the in vitro function and in vivo reendothelialization capability of EPCs were suppressed. Is 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. Ese findings further indicate that aliskiren is an effective pharmacological treatment for cell-based repair in hypertension-related vascular injury Conclusions. is 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. ese findings further indicate that aliskiren is an effective pharmacological treatment for cell-based repair in hypertension-related vascular injury
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