Ezrin knockdown reduces procaterol-stimulated ciliary beating without morphological changes in mouse airway cilia

Author:

Kawaguchi Kotoku1ORCID,Nakayama Shogo2,Saito Daichi1,Kogiso Haruka3,Yasuoka Kasane1,Marunaka Yoshinori345,Nakahari Takashi3ORCID,Asano Shinji13ORCID

Affiliation:

1. Department of Molecular Physiology, College of Pharmaceutical Sciences, Ritsumeikan University, Shiga 525-8577, Japan

2. Laboratory for Lung Development and Regeneration, Riken Center for Biosystems Dynamics Research (BDR), Kobe 650-0047, Japan

3. Research Unit for Epithelial Physiology, Research Organization of Science and Technology, Ritsumeikan University, Shiga 525-8577, Japan

4. Department of Molecular Cell Physiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan

5. Medical Research Institute, Kyoto Industrial Health Association, Kyoto 604-8472, Japan

Abstract

ABSTRACT Mucociliary clearance, which is conducted by beating cilia cooperating with the surface mucous layer, is a major host defense mechanism of the airway epithelium. Ezrin, a crosslinker between membrane proteins and the actin cytoskeleton, is located in microvilli and around the basal bodies in airway ciliary cells. It is also likely that ezrin plays an important role in apical localization of β2 adrenergic receptor (β2AR) in airway ciliary cells. Here, we studied the physiological roles of ezrin by using trachea and airway epithelial cells prepared from ezrin-knockdown (Vil2kd/kd) mice. The trachea and airway ciliary cells of Vil2kd/kd mice presented a normal morphology and basal body orientation, suggesting that ezrin is not directly involved in development and planar cell polarity of cilia. Procaterol stimulates ciliary beating (frequency and amplitude) via β2AR in the airway ciliary cells. In the Vil2kd/kd mice, airway ciliary beating stimulated with procaterol was partly inhibited due to the impairment of cell surface expression of β2AR. These results suggest that ezrin regulates the beating of airway ciliary cells by promoting the apical surface localization of β2AR. This article has an associated First Person interview with the first author of the paper.

Funder

Japan Society for the Promotion of Science

Ministry of Education, Culture, Sports, Science and Technology

Takeda Science Foundation

Publisher

The Company of Biologists

Subject

Cell Biology

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