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布拉迪基宁缺乏导致小鼠高血压
Yusuke Ohnaka1, Satoshi Tsukamoto2, Yuna Iwai1
1Laboratory of Molecular Cellular Biology, School of Pharmaceutical Sciences, Kobe Gakuin University, 1-1-3 Minatojima, Chuo-ku, Kobe, 650-8586, Japan.
Biochemical and biophysical research communications
|September 27, 2023
概括
研究人员创造了突变小鼠来研究布拉迪基宁 (BK). 这些小鼠表现出血激素降低和血压升高,这表明激素激素.
科学领域:
- 生理学 生理学 生理学
- 遗传学 是一个遗传学.
- 心血管生物学 心血管生物学
背景情况:
- 布拉迪基宁 (BK) 在血管扩张和血压调节中起作用.
- BK的精确生理功能尚未完全阐明.
- 基尼诺基因是kallikrein-kinin系统中的一个前体蛋白.
研究的目的:
- 为了研究血激素在血压调节中的作用.
- 了解金素对血管kallikrein-kinin系统的贡献.
主要方法:
- 使用CRISPR/Cas9基因编辑生成BKdelK1和BKdelK2突变小鼠.
- 在小鼠kininogen1和kininogen2基因的BK部分引入了向突变.
- 血激素水平和素释放的BK被量化并与突变和野生型 (WT) 小鼠进行比较.
主要成果:
- BKdelK1和BKdelK2突变小鼠表现出大约50%的低分子量激素在血中的减少.
- 与WT相比,素释放的BK水平在突变小鼠中也减少了约50%.
- 与WT小鼠相比,BKdelK1和BKdelK2小鼠都显示出显著升高的缩血压.
结论:
- 血低分子量基因素 (LKNG) 在血管卡利克莱因-基因系统中作为基因素 (KNG) 的关键来源.
- 血LKNG的减少有助于增加缩血压.
- 这些发现凸显了原-素通路在维持正常血压方面的重要性.
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