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
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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