Hiob Matti A, Trane Andy E, Wise Steven G, Bernatchez Pascal N, Weiss Anthony S
School of Life & Environmental Biosciences, University of Sydney, Sydney, NSW 2006, Australia.
Charles Perkins Centre, University of Sydney, Sydney, NSW 2006, Australia.
Nanomedicine (Lond). 2016 Jun;11(12):1591-7. doi: 10.2217/nnm-2016-0052. Epub 2016 May 13.
This study aimed to characterize the role of tropoelastin in eliciting a nitric oxide response in endothelial cells.
Nitric oxide production in cells was quantified following the addition of known nitric oxide synthase pathway inhibitors such as LNAME and 1400W. The effect of eNOS siRNA knockdowns was studied using western blotting and assessed in the presence of PI3K-inhibitor, wortmannin.
Tropoelastin-induced nitric oxide production was LNAME and wortmannin sensitive, while being unaffected by treatment with 1400W.
Tropoelastin acts through a PI3K-specific pathway that leads to the phosphorylation of eNOS to enhance nitric oxide production in endothelial cells. This result points to the benefit of the use of tropoelastin in vascular applications, where NO production is a characteristic marker of vascular health.
本研究旨在表征原弹性蛋白在内皮细胞中引发一氧化氮反应的作用。
在添加已知的一氧化氮合酶途径抑制剂(如LNAME和1400W)后,对细胞中一氧化氮的产生进行定量。使用蛋白质免疫印迹法研究内皮型一氧化氮合酶(eNOS)小干扰RNA敲低的效果,并在磷脂酰肌醇-3-激酶(PI3K)抑制剂渥曼青霉素存在的情况下进行评估。
原弹性蛋白诱导的一氧化氮产生对LNAME和渥曼青霉素敏感,而不受1400W处理的影响。
原弹性蛋白通过PI3K特异性途径发挥作用,该途径导致eNOS磷酸化,从而增强内皮细胞中一氧化氮的产生。这一结果表明在血管应用中使用原弹性蛋白的益处,其中一氧化氮的产生是血管健康的特征性标志物。