牙龈卟啉单胞菌
蛋白激酶B
福克斯O1
伊诺斯
血管生成
化学
免疫印迹
磷酸化
癌症研究
细胞生物学
生物
内科学
一氧化氮合酶
内分泌学
医学
牙周炎
一氧化氮
生物化学
基因
作者
Hui Deng,Yixuan Gong,Yuan Chen,Guigui Zhang,Hui Chen,Tianfan Cheng,Lijian Jin,Yi Wang
摘要
Endothelial progenitor cells (EPCs) function as the angiogenic switch of many physiological and pathological conditions. We aimed to investigate the effects of Porphyromonas gingivalis lipopolysaccharide on the angiogenic capacity of EPCs and delineate the underlying mechanisms.EPCs were isolated from human umbilical blood. CCK-8 assay was undertaken to analyze the cell viability. The migration and tube formation capacity were assessed by wound healing and tube formation, respectively. The protein expression of Akt/p-Akt, endothelial nitric oxide synthase (eNOS)/p-eNOS, and Forkhead box O1 (FoxO1)/p-FoxO1 was determined by Western blot. The intracellular localization of FoxO1 was evaluated by immunofluorescent staining.P. gingivalis LPS at 10 μg/ml significantly increased the viability (10.9 ± 2.9%), migration (16.3 ± 3.1%), and tube formation (38.6 ± 5.5%) of EPCs, along with increased phosphorylation of Akt, eNOS, and FoxO1. Mechanistically, Akt inhibition by specific inhibitor wortmannin and FoxO1 forced expression by adenovirus transfection in EPCs markedly attenuated the P. gingivalis LPS-induced eNOS activation, tube formation, and migration. Moreover, P. gingivalis LPS-induced phosphorylation and nuclear exclusion of FoxO1 were blunted by Akt inhibition.The present study suggests that P. gingivalis LPS could affect the angiogenic function of EPCs through the Akt/FoxO1 signaling. The current findings may shed light on the clinical association of periodontitis with aberrant angiogenesis seen in atherosclerotic plaque rupture.
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