Acute mental tress-induced modulation of aortic endothelial cells in mice

Mental stress is a substantial contributor to human disease initiation and progression, including cardiovascular pathologies. However, the underlying mechanisms remain largely unclear. Here, we show in mice that acute mental stress enhances influx of leukocytes into atherosclerotic plaques through modulation of endothelial cells. Specifically, acute stress increases adhesion molecule expression and chemokines release through locally derived norepinephrine. Overall design: Here, we tested whether acute mental stress activates endothelial cells and consequently promotes influx of leukocytes in mice. We applied acute mental stress to ApoE mice for each 3 h on 3 consecutive days and excised aortae afterwards. To get a broader understanding which phenotypic changes endothelial cells undergo in response to acute stress, we FACS (fluorescence-activated cell sorting) isolated aortic endothelial cells from stressed vs. non-stressed mice and subjected them to RNA sequencing.

精神压力是人类疾病发生与进展的重要诱因，涵盖心血管病理状态，但其潜在作用机制在很大程度上仍不明确。本研究通过小鼠实验证实，急性精神压力可通过调控内皮细胞，促进白细胞向动脉粥样硬化斑块内浸润。具体而言，急性压力可通过局部释放的去甲肾上腺素上调黏附分子表达并促进趋化因子释放。
实验设计概述：本研究旨在验证急性精神压力是否可激活小鼠体内的内皮细胞，并进而促进白细胞浸润。我们对载脂蛋白E（ApoE）小鼠连续3天每日施加3小时急性精神压力刺激，随后摘取主动脉组织。为全面解析内皮细胞在急性压力刺激下的表型变化，我们通过荧光激活细胞分选（Fluorescence-activated cell sorting, FACS）分别从施加压力与未施加压力的小鼠体内分离主动脉内皮细胞，并对其开展RNA测序分析。