失重引起的机体心血管功能失调是制约长期载人航天飞行的重要因素，血管内皮细胞功能异常在失重后心血管失调中扮演重要角色，但其机理尚未明确。膜-骨架连接蛋白moesin已证实在调控细胞骨架分布和细胞功能中发挥重要作用。我课题组前期研究发现，模拟失重可致moesin上游调控分子RhoA/ROCK活性增强，证实失重所致的动脉收缩功能异常与RhoA活性增强有关。据此我们推测，RhoA/ROCK介导moesin活性增高可能是调控失重后内皮细胞功能异常的重要通路。本课题拟在前期研究基础上，以大血管和微血管内皮细胞为研究对象，应用细胞及动物模拟失重模型，探讨模拟失重致内皮细胞功能异常的变化规律，揭示meosin在失重后内皮细胞骨架分布异常及功能改变中的作用，阐明模拟失重致内皮细胞meosin异常表达的分子机制。该结果有助于完善失重致血管内皮细胞功能变化的可能机制，为防护失重致机体心血管功能失调提供新的依据。

The cardiovascular dysfunction induced by microgravity is thought to represent one of the dangers of long term spaceflight. It has been shown that changes of endothelial cells function appear to be play important role in cardiovascular deconditioning. Yet, the cellular and molecular mechanism underlying it remains to be fully elucidated. Moesin is emerging as the potential candidate that likely to mediate this process. Serving as cross-linkers between actin filaments and plasma membrane, moesin is engaged in cytoskeleton redistribution and cell functions. Our previous study shows that altered expression and activity of RhoA/ROCK may play important roles in the increased vasoconstriction of thoracic aorta induced by simulated microgravity in rats. Differences of the thoracic aortic vasoconstriction between simulatedm icrogravity and normal rats could be eliminated by inhibition of ROCK. Therefore, we presume the RhoA-ROCK-dependent moesin phosphoryaltion is involved in endothelium dysfunctions induced by simulated microgravity. In this study, we will use the clinostat and tail-suspended rats to simulate microgravity. The aim of this study is to explore the changes of endothelial cells function induced by simulated microgravity, and further to elucidate the role of moesin in regulating cytoskeleton distribution and cell functions after microgravity exposure and the mechanisms underlying it. Our finding might help to know the possible mechanism of the endothelium dysfunctions induced by microgravity and provide some theoretical basis to the protection of postflight cardiovasucular dysfunctions.