Regulation of ciliary beat frequency by the nitric oxide signaling pathway in mouse nasal and tracheal epithelial cells

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cilia / metabolism*
  • Epithelial Cells / metabolism*
  • Mice
  • Mice, Inbred BALB C
  • Nasal Mucosa / cytology*
  • Nitric Oxide / metabolism*
  • Signal Transduction*
  • Trachea / cytology*


  • Nitric Oxide