ArticleThe Journal of physiology2003
The role of cGMP in the regulation of rabbit airway ciliary beat frequency.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 53 citations in OpenAlex.
- T2R38 taste receptor polymorphisms underlie susceptibility to upper respiratory infection.The Journal of clinical investigation · 2012Trial
- Respiratory Ciliary Beat Frequency in COPD: Balancing Oxidative Stress and Pharmacological Treatment.Antioxidants (Basel, Switzerland) · 2025Review
- First contact: the role of respiratory cilia in host-pathogen interactions in the airways.American journal of physiology. Lung cellular and molecular physiology · 2020Review
- Ciliary beating amplitude controlled by intracellular ClPflugers Archiv : European journal of physiology · 2019Article
- Broncho-Vaxom® (OM-85 BV) soluble components stimulate sinonasal innate immunity.International forum of allergy & rhinology · 2019Article
- CALHM1-Mediated ATP Release and Ciliary Beat Frequency Modulation in Nasal Epithelial Cells.Scientific reports · 2017Article
- Review
- Cyclic GMP and Cilia Motility.Cells · 2015Review
- Methods to measure and analyze ciliary beat activity: Ca2+ influx-mediated cilia mechanosensitivity.Pflugers Archiv : European journal of physiology · 2012Article
- Computational modelling elucidates the mechanism of ciliary regulation in health and disease.BMC systems biology · 2011Article
- Regulation of ciliary motility: conserved protein kinases and phosphatases are targeted and anchored in the ciliary axoneme.Archives of biochemistry and biophysics · 2011Review
- A role for p38 MAPK in the regulation of ciliary motion in a eukaryote.BMC cell biology · 2011Article
- In vitro culturing of porcine tracheal mucosa as an ideal model for investigating the influence of drugs on human respiratory mucosa.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2008Article
- Apical oxidative hyaluronan degradation stimulates airway ciliary beating via RHAMM and RON.American journal of respiratory cell and molecular biology · 2007Article
- Ciliary beat frequency is maintained at a maximal rate in the small airways of mouse lung slices.American journal of respiratory cell and molecular biology · 2006Article
- Intracellular Ca2+ regulates the phosphorylation and the dephosphorylation of ciliary proteins via the NO pathway.The Journal of general physiology · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The involvement of cyclic guanosine 3',5'-monophosphate (cGMP) and cGMP-dependent protein kinase (PKG) and their interaction with the Ca2+-dependent mechanisms in the regulation of ciliary activity are not well understood. To investigate how cGMP regulates ciliary activity, changes in ciliary beat frequency (CBF) and intracellular calcium concentration ([Ca2+]i) of rabbit tracheal ciliated cells in response to 8-bromo-cGMP (Br-cGMP) were simultaneously quantified using digital, high-speed phase-contrast and fluorescence imaging. Br-cGMP induced a response in ciliary activity that could be separated into two parts. Firstly, Br-cGMP induced a concentration-dependent increase in the basal CBF that occurred without increasing the [Ca2+]i. This response was not affected by excessively buffering the [Ca2+]i with BAPTA but was abolished by KT5823, a PKG inhibitor. Secondly, Br-cGMP induced a series of transient increases in CBF that were superimposed on the sustained increases in CBF. These transient increases in CBF correlated with the stimulation of a series of transient increases in [Ca2+]i and were abolished by BAPTA, but were unaffected by KT5823. The magnitude of the transient increases in CBF and [Ca2+]i were not dependent on the concentration of Br-cGMP. The Ca2+-dependent changes in CBF induced by ionomycin or ATP were not affected by KT5823. From these results, we propose that cGMP increases CBF in two ways: firstly through a Ca2+-independent mechanism involving PKG, and secondly through a Ca2+-dependent mechanism following the stimulation of changes in [Ca2+]i. In addition, we suggest that the Ca2+-dependent stimulation of rabbit airway ciliary activity does not initially require PKG activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.