Related Experiment Video
Updated: Jan 16, 2026
11:13
Collection, Expansion, and Differentiation of Primary Human Nasal Epithelial Cell Models for Quantification of Cilia Beat Frequency
Published on: November 10, 2021
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17β-estradiol (E2) increases ciliary beat frequency via membrane estrogen receptor β
Kouta Noriyama1, Nobuhisa Todo1, Nobuyo Tamiya2
1Laboratory of Clinical and Translational Physiology, Kyoto Pharmaceutical University, 5 Nakauchi-cho, Misasagi, Yamashina-ku, Kyoto 607-8414, Japan.
The Journal of Steroid Biochemistry and Molecular Biology
|October 1, 2025
Summary
Estrogen (E2) boosts airway ciliated cell function by increasing ciliary beat frequency (CBF) and cAMP levels. This effect is mediated through membrane estrogen receptor beta (ERβ), enhancing mucociliary clearance.
Area of Science:
- Respiratory Physiology
- Endocrinology
- Cell Biology
Background:
- Estrogen receptors (ER) are present in respiratory tissues, but estrogen's role in airway ciliated cells is largely unknown.
- Airway ciliated cells are crucial for mucociliary clearance (MCC), with ciliary beat frequency (CBF) indicating MCC efficiency.
Purpose of the Study:
- To investigate the effect of 17β-estradiol (E2) on ciliary beat frequency (CBF) in murine airway ciliated cells.
- To elucidate the specific estrogen receptor (ER) pathway involved in E2's action on CBF.
Main Methods:
- Measurement of CBF and intracellular cAMP concentration ([cAMP]i) in response to E2.
- Utilized selective ERβ inhibitor (PHTPP) and membrane-impermeable E2 conjugate to probe receptor involvement.
- Assessed effects on intracellular Ca2+ and pH.
Main Results:
- E2 significantly increased CBF and [cAMP]i in murine airway ciliated cells.
- ERβ inhibition (PHTPP) blocked E2-induced increases in CBF and [cAMP]i.
- Membrane-impermeable E2 also increased CBF and [cAMP]i, further implicating membrane ERβ.
Conclusions:
- 17β-estradiol enhances ciliary beat frequency via increased intracellular cAMP through membrane ERβ in airway ciliated cells.
- This study reveals a novel mechanism for estrogen action in the respiratory tract, impacting mucociliary clearance.
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