期刊
EXPERIMENTAL CELL RESEARCH
卷 317, 期 17, 页码 2548-2553出版社
ELSEVIER INC
DOI: 10.1016/j.yexcr.2011.07.007
关键词
Cilia; Nitric oxide; Signaling pathway; Mouse; Nasal; Tracheal
资金
- National Science Fund for Distinguished Young Scholars [81025007]
- National Natural Science Foundation of China [30872846, 30973282]
- Beijing Science and Technology Program [KZ200910025008]
- Beijing Natural Science Foundation [7102030]
- Special Fund of Sanitation Elite Reconstruction of Beijing [2009-2-007]
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 beta, PKG I and acetylated a 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 CL-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 beta 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 eN0S-NO-sGC beta-cGMP-PKG I pathway. (C) 2011 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据