一氧化氮信号通路对小鼠鼻腔和气管上皮细胞纤毛摆动频率的调控。
Regulation of ciliary beat frequency by the nitric oxide signaling pathway in mouse nasal and tracheal epithelial cells.
机构信息
Key Laboratory of Otolaryngology, Head and Neck Surgery (Ministry of Education), Beijing Institute of Otolaryngology, China.
出版信息
Exp Cell Res. 2011 Oct 15;317(17):2548-53. doi: 10.1016/j.yexcr.2011.07.007. Epub 2011 Jul 20.
OBJECTIVES
Our purpose was to investigate the role of the nitric oxide (NO) signaling pathway in the regulation of ciliary beat frequency (CBF) in mouse nasal and tracheal epithelial cells.
METHODS
We studied the effects of the NO donor l-arginine (L-Arg) and specific inhibitors of the NO signaling pathway on CBF of both nasal and tracheal epithelial cells by using high-speed digital microscopy. We also examined eNOS, sGC β, PKG I and acetylated α tubulin expression in native mouse nasal and tracheal epithelium using immunohistochemical methods.
RESULTS
L-Arg significantly increased CBF of cultured nasal and tracheal epithelial cells, and the effects were blocked by pretreatment with N(G)-nitro-l-arginine methyl ester (L-NAME), a NOS inhibitor, with LY-83583, a sGC inhibitor, or with KT-5823, a PKG inhibitor. Positive immunostaining for NO signaling molecules including eNOS, sGC β and PKG I was observed in either nasal or tracheal ciliated epithelium.
CONCLUSION
NO plays a role in regulating CBF of mouse respiratory epithelial cells via a eNOS-NO-sGC β-cGMP-PKG I pathway.
目的
本研究旨在探讨一氧化氮（NO）信号通路在调节小鼠鼻和气管上皮细胞纤毛摆动频率（CBF）中的作用。
方法
我们采用高速数字显微镜技术研究了NO 供体 l-精氨酸（L-Arg）和特定的 NO 信号通路抑制剂对鼻和气管上皮细胞 CBF 的影响。我们还使用免疫组织化学方法检测了天然状态下的小鼠鼻和气管上皮细胞中内皮型一氧化氮合酶（eNOS）、可溶性鸟苷酸环化酶 β 亚基（sGC β）、蛋白激酶 G I（PKG I）和乙酰化α 微管蛋白的表达。
结果
L-Arg 显著增加了培养的鼻和气管上皮细胞的 CBF，NOS 抑制剂 N(G)-硝基-l-精氨酸甲酯（L-NAME）、sGC 抑制剂 LY-83583 或 PKG 抑制剂 KT-5823 预处理可阻断这一作用。eNOS、sGC β 和 PKG I 等 NO 信号分子在鼻或气管纤毛上皮中均有阳性免疫染色。
结论
NO 通过 eNOS-NO-sGC β-cGMP-PKG I 通路在调节小鼠呼吸上皮细胞 CBF 中发挥作用。
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