Muscarinic Receptors and BK Channels Are Affected by Lipid Raft Disruption of Salivary Gland Cells
Autor: | La-Mee Choi, Yoon-Jung Kim, Jisoo Lee, Hee-Kyung Park, Se-Young Choi, Keimin Lee |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
BK channel Thapsigargin QH301-705.5 aquaporin-5 salivary gland Catalysis Article Salivary Glands Cell Line Inorganic Chemistry 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Membrane Microdomains Muscarinic acetylcholine receptor Humans Secretion Large-Conductance Calcium-Activated Potassium Channels Physical and Theoretical Chemistry Transcellular Biology (General) Molecular Biology Lipid raft QD1-999 Spectroscopy Ion channel G protein-coupled receptor biology Chemistry Organic Chemistry Water General Medicine Receptors Muscarinic Computer Science Applications Cell biology lipid raft 030104 developmental biology G-protein coupled receptor biology.protein lipids (amino acids peptides and proteins) methyl-beta-cyclodextrin 030217 neurology & neurosurgery |
Zdroj: | International Journal of Molecular Sciences, Vol 22, Iss 4780, p 4780 (2021) International Journal of Molecular Sciences Volume 22 Issue 9 |
ISSN: | 1661-6596 1422-0067 |
Popis: | Activity-dependent fluid secretion is the most important physiological function of salivary glands and is regulated via muscarinic receptor signaling. Lipid rafts are important for G-protein coupled receptor (GPCR) signaling and ion channels in plasma membranes. However, it is not well understood whether lipid raft disruption affects all membrane events or only specific functions in muscarinic receptor-mediated water secretion in salivary gland cells. We investigated the effects of lipid raft disruption on the major membrane events of muscarinic transcellular water movement in human salivary gland (HSG) cells. We found that incubation with methyl-β-cyclodextrin (MβCD), which depletes lipid rafts, inhibited muscarinic receptor-mediated Ca2+ signaling in HSG cells and isolated mouse submandibular acinar cells. However, MβCD did not inhibit a Ca2+ increase induced by thapsigargin, which activates store-operated Ca2+ entry (SOCE). Interestingly, MβCD increased the activity of the large-conductance Ca2+-activated K+ channel (BK channel). Finally, we found that MβCD did not directly affect the translocation of aquaporin-5 (AQP5) into the plasma membrane. Our results suggest that lipid rafts maintain muscarinic Ca2+ signaling at the receptor level without directly affecting the activation of SOCE induced by intracellular Ca2+ pool depletion or the translocation of AQP5 into the plasma membrane. |
Databáze: | OpenAIRE |
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