Microvascular endothelial control of bone metabolism in rats: nitric oxide and endothelin systems

以下是我目前研究项目的总结。内皮素/内皮素受体亚型A系统在骨代谢控制中的作用（文献#3）我们发现，长期阻断内皮素A受体可减少生长大鼠的骨形成并诱导骨质减少。这表明血管内皮细胞产生的内皮素在骨生长和体内代谢中起重要作用。血管内皮细胞功能的氧化还原调节（文献#4）。6,7)利用电细胞-基质阻抗传感器技术，我们观察到一氧化氮（NO）调节人微血管内皮细胞的细胞-基质和/或细胞-细胞粘附，并提示NO可能改变人微血管通透性。我们还发现了组成型NO合成酶活性在维持大鼠氧化缓冲能力中的重要性。内皮细胞功能障碍的病理生理学（参考文献#5）我们总结了我们最近的观察结果，表明病理状态（如动脉粥样硬化、高血压和心力衰竭）对血管生成刺激的不适当反应中NO产生不足。婴儿代谢性骨病的骨代谢评估我们首次证明了低骨转换状态存在于婴儿骨质减少不完全型3中。

The following is the summary of my current research project.1. Role of endothelin/endothelin receptor subtype A system in the control of bone metabolism (Reference #3)We found that the long-term blockade of the endothelin A receptor reduces bone formation and induces osteopenia in growing rats. This result suggests that endothelin produced by vascular endothelial cells plays an important role in bone growth and metabolism in vivo.2. Redox modulation of vascular endothelial cell function (Reference #4. 6, 7)Using the electrical cell-substrate impedance sensor technique, we observed that nitric oxide (NO) modulates cell-matrix and/or cell-cell adhesion in human microvascular endothelial cells and suggested that NO might modify microvascular permeability in humans. We also found the importance of the constitutive NO synthase activity in the maintenance of oxidant buffering capacity in rats.3. Pathophysiology of endothelial cell dysfunction (Reference #5)We have summarized our recent observations implicating insufficient NO production in pathological states (e.g., atherosclerosis, hypertension and heart failure) in the inappropriate response to angiogenic stimuli.4. Assessment of bone metabolism in infantile metabolic bone diseasesWe demonstrated for the first time that the low bone turnover state lies in the infantile osteopenia imperfecta type3.