Acetylcholine-induced ex vivo ATP release from the human nasal mucosa

Koizumi, Hiroki; Ikezaki, Shoji; Ohbuchi, Toyoaki; Hung, Ba; Hohchi, Nobusuke; Kawaguchi, Rintaro; Kitamura, Takuro; Suzuki, Hideaki

doi:10.1016/j.anl.2016.09.003

Auris Nasus Larynx

2017

DOI: 10.1016/j.anl.2016.09.003

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Acetylcholine-induced ex vivo ATP release from the human nasal mucosa

Hiroki Koizumi

Shoji Ikezaki

Toyoaki Ohbuchi

et al.

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Cited by 10 publications

(11 citation statements)

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“…Our recent ex vivo study has shown that Ach induces ATP release from the human nasal mucosa. 15 We found that this reaction is strongly dependent on extracellular Ca 2þ and mediated by the inositol 1,4,5-trisphosphate (IP 3 ) receptor, pannexin-1 channel, and purinergic P2X7 receptor. 15 However, how this reaction connects with airway epithelial functions has been unknown.…”

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confidence: 98%

“…15 We found that this reaction is strongly dependent on extracellular Ca 2þ and mediated by the inositol 1,4,5-trisphosphate (IP 3 ) receptor, pannexin-1 channel, and purinergic P2X7 receptor. 15 However, how this reaction connects with airway epithelial functions has been unknown. Considering that Ach, ATP, and Ca 2þ are substances which stimulate ciliary movement, we formulated a hypothesis that this Ach-induced reaction pathway for ATP release is involved in the regulation of the ciliary beat.…”

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confidence: 98%

“…4 Extracellular release of ATP is thought to be mediated by 2 different mechanisms: vesicle-and channel-mediated modes. 15 Among a number of channels that may be involved in the extracellular release of ATP in various types of cells, including airway epithelial cells, the pannexin-1 channel is one of the most convincing candidates. 16 The pannexin-1 channel-mediated mode is actually the major mechanism of the extracellular ATP release in the human nasal mucosa, whereas the vesicle-mediated mode does not participate in this reaction.…”

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confidence: 99%

“…16 The pannexin-1 channel-mediated mode is actually the major mechanism of the extracellular ATP release in the human nasal mucosa, whereas the vesicle-mediated mode does not participate in this reaction. 15 Muscarinic agonists such as Ach are other substances that upregulate the ciliary beat in the upper and lower airway epithelium. 1,[17][18][19] Despite a number of previous studies, the intracellular signaling pathway that controls the ciliary beat remains unclear.…”

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confidence: 99%

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Acetylcholine-induced Ciliary Beat of the Human Nasal Mucosa Is Regulated by the Pannexin-1 Channel and Purinergic P2X Receptor

Ohbuchi

Wakasugi

et al. 2018

Am J Rhinol�Allergy

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These results indicate that the regulatory mechanism of the Ach-induced ciliary beat is dependent on extracellular Ca and involves the muscarinic Ach receptor, IP receptor, pannexin-1 channel, purinergic P2X receptor, and connexin channel. We proposed a tentative intracellular signaling pathway of the Ach-induced ciliary beat, in which the pannexin-1-P2X unit may play a central role in ciliary beat regulation.

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confidence: 98%

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confidence: 98%

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confidence: 99%

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confidence: 99%

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Acetylcholine-induced Ciliary Beat of the Human Nasal Mucosa Is Regulated by the Pannexin-1 Channel and Purinergic P2X Receptor

Ohbuchi

Wakasugi

et al. 2018

Am J Rhinol�Allergy

Self Cite

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“…In calcium-dependent activation, pannexin-1 channel opening is evoked by signal transduction events following the activation of the ionotropic purinergic P2 x 7 receptor, which is directly coupled with the pannexin-1 channel [ 12 , 16 , 23 ]. Activation of the acetylcholine receptor and transient receptor potential vanilloid 1 (TRPV1) also induces ATP release by pannexin-1 in nasal mucosa [ 21 , 22 ]. In calcium-independent activation, the pannexin-1 channel is triggered by mechanical stimulation, such as hypotonic stress-induced cell swelling and membrane stretching [ 2 , 13 , 20 , 24 – 26 ].…”

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confidence: 99%

Synchronized roles of pannexin and connexin in nasal mucosal epithelia

Ohbuchi

Suzuki

2018

Eur Arch Otorhinolaryngol

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BackgroundNasal mucosal epithelial cells express connexins, the prototypical gap junction proteins, and pannexins, a new family of channel proteins homologous to the invertebrate gap junction proteins. The physiological and pathophysiological roles of these transmembrane proteins in nasal mucosa are largely still unknown.PurposePannexins participate in ATP release into the extracellular space in various tissues, and ATP plays important roles in mucociliary clearance, especially by regulating ciliary beat activity. Therefore, we focused on the functional relationship between connexins, pannexin-1, ATP release, and mucociliary clearance in nasal epithelia.Results and ConclusionsConnexins participate in the generation of intercellular calcium waves, in which calcium-mediated signaling responses spread to contiguous cells through the gap junction formed by connexins to transmit calcium signaling throughout the airway epithelium. Pannexins in the nasal mucosa may contribute to not only ciliary beat modulation via ATP release, but also regulation of mucus blanket components via H2O efflux. The synchronized roles of pannexin and connexin may provide a new insight into effective mucociliary clearance systems in nasal mucosa.

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TRPA1/M8 agonists upregulate ciliary beating through the pannexin-1 channel in the human nasal mucosa

et al. 2022

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Background Nasal breathing is important for maintaining physiological respiration. However, airflow in the nasal cavity has an inherent cooling effect and may suppress ciliary beating, an essential frontline defense in the airway. Nasal airflow is thought to be perceived by thermoreceptors for cool temperatures. We herein investigated the effect of the activation of thermosensitive transient receptor potentials (TRPs) for cool/cold temperatures on ciliary beating to search for a compensatory mechanism. Methods Inferior turbinates were collected from patients with chronic hypertrophic rhinitis. Ex vivo ciliary beat frequency (CBF) and ATP release were measured using a high-speed digital video camera and by luciferin-luciferase assay, respectively. Intracellular Ca2+ ([Ca2+]i) imaging of isolated ciliated cells was performed using Fluo-8. The nasal mucosae were also subjected to fluorescence immunohistochemistry and real-time RT-PCR for TRPA1/TRPM8. Results CBF was significantly increased by adding either cinnamaldehyde (TRPA1 agonist) or l-menthol (TRPM8 agonist). This increase was inhibited by pannexin-1 blockers, carbenoxolone and probenecid. Cinnamaldehyde and l-menthol also increased the ATP release from the nasal mucosa and [Ca2+]i of isolated ciliated cells. Immunohistochemistry detected TRPA1 and TRPM8 on the epithelial surface including the cilia and in the submucosal nasal glands. Existence of these receptors were confirmed at the transcriptional level by real-time RT-PCR. Conclusions These results indicate the stimulatory effect of the activation of TRPA1/TRPM8 on ciliary beating in the nasal mucosa, which would be advantageous to maintain airway mucosal defense against the fall of temperature under normal nasal breathing. This stimulatory effect is likely to be mediated by pannexin-1.

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Acetylcholine-induced ex vivo ATP release from the human nasal mucosa

Cited by 10 publications

References 27 publications

Acetylcholine-induced Ciliary Beat of the Human Nasal Mucosa Is Regulated by the Pannexin-1 Channel and Purinergic P2X Receptor

Acetylcholine-induced Ciliary Beat of the Human Nasal Mucosa Is Regulated by the Pannexin-1 Channel and Purinergic P2X Receptor

Synchronized roles of pannexin and connexin in nasal mucosal epithelia

TRPA1/M8 agonists upregulate ciliary beating through the pannexin-1 channel in the human nasal mucosa

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