雷宁- ангиотензин系统介导的氧化物信号传递在受体细胞中
Marharyta Semenikhina1, Ruslan Bohovyk2, Mykhailo Fedoriuk1
1Division of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, United States.
American journal of physiology. Renal physiology
|July 18, 2024
概括
氨酸- ангиотензин系统通过氨酸II型2受体 (AT2R) 激活氧化物 (NO) 在细胞中的产生,从而影响信号传递和细胞结构.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 氧化 (NO) 调节功能和血压.
- 在上皮细胞,特别是细胞中NO作用的机制尚未完全理解.
- 之前的研究已经确定了 ангиотензин II (ANG II),而不是ATP是细胞中NO信号的发起者.
研究的目的:
- 为了研究氨酸-血管新生素系统 (RAS) 和细胞中NO的产生之间的相互作用.
- 为了阐明涉及RAS介导的NO生成的特定受体和信号通路在 podocytes.
- 了解NO信号如何影响细胞结构和功能.
主要方法:
- 使用培养的人类 podocytes 和隔离的老鼠球粒.
- 使用了共聚焦显微镜和扫描探针显微镜.
- 检测NO产量,NO/Ca2+交叉,F-actin动态,和 podocyte 形态. 检测NO产量,NO/Ca2+交叉,F-actin动态和 podocyte 形态.
主要成果:
- ANG II 和 ANG III 激活了血管激素II 2 型受体 (AT2R),从而产生显著的NO水平.
- ANG 1-7的中度NO反应也通过AT2R进行介导;没有检测到MAS受体.
- 的产生调节了细胞内Ca2+信号传递,增加了细胞体积,并通过AT2R驱动了lamellipodia突出.
结论:
- 在 podocytes 中的 AT2R 激活显著增强了 NO 生产.
- 这种NO的产生影响了细胞内Ca2+的动态和 podocyte 的体积和生长.
- 这些RAS-NO介导的机制在生理和病理生理状态下对 podocyte 功能至关重要.
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