Kidney international · 2005
Aldosterone makes human endothelium stiff and vulnerable.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Oberleithner Hans
Аннотация
BACKGROUND: Aldosterone has long been known to control water and electrolyte balance by acting on mineralocorticoid receptors in kidney. However, recent studies identified these classic receptors also in the vascular system. Indeed, aldosterone alters structure and function of human endothelium. We applied nanotechniques to detect these changes.
METHODS: Experiments were performed in cultured monolayers of human umbilical vein endothelial cells (HUVECs). Ten nanomoles per liter aldosterone or solvent (control) was added to the culture medium for 72 hours. Atomic force microscopy (AFM) was used as a nanotool that physically interacts with the cell surface. In the monolayer we measured cell volume, apical cell surface, and cell stiffness.
RESULTS: Volume, apical surface area, and stiffness of individual cells increased in response to aldosterone by 18% (P < 0.05), 64% (P < 0.001), and 78% (P < 0.01), respectively. Imaging of the cell-to-cell contacts disclosed gaps in response to aldosterone. Furthermore, underneath the monolayer we detected an aldosterone-induced increase of protein deposition by 58% (P < 0.001).
CONCLUSION: Aldosterone remodels human endothelium in vitro. Cells increase in size and stiffness. Protein leakage through intercellular gaps could be caused by the increased apical membrane tension. The increase in cell rigidity could trigger endothelial dysfunction observed in hyperaldosteronism.
METHODS: Experiments were performed in cultured monolayers of human umbilical vein endothelial cells (HUVECs). Ten nanomoles per liter aldosterone or solvent (control) was added to the culture medium for 72 hours. Atomic force microscopy (AFM) was used as a nanotool that physically interacts with the cell surface. In the monolayer we measured cell volume, apical cell surface, and cell stiffness.
RESULTS: Volume, apical surface area, and stiffness of individual cells increased in response to aldosterone by 18% (P < 0.05), 64% (P < 0.001), and 78% (P < 0.01), respectively. Imaging of the cell-to-cell contacts disclosed gaps in response to aldosterone. Furthermore, underneath the monolayer we detected an aldosterone-induced increase of protein deposition by 58% (P < 0.001).
CONCLUSION: Aldosterone remodels human endothelium in vitro. Cells increase in size and stiffness. Protein leakage through intercellular gaps could be caused by the increased apical membrane tension. The increase in cell rigidity could trigger endothelial dysfunction observed in hyperaldosteronism.