Activation of acetylcholine receptor elicits intracellular Ca2+ mobilization, transient cytotoxicity, and induction of RANKL expression
International Journal of Oral Biology
; : 119-123, 2016.
Article
in Ko
| WPRIM
| ID: wpr-124491
Responsible library:
WPRO
ABSTRACT
Acetylcholine receptors (AChR) including muscarinic and nicotinic AChR are widely expressed and mediate a variety of physiological cellular responses in neuronal and non-neuronal cells. Notably, a functional cholinergic system exists in oral epithelial cells, and nicotinic AChR (nAChR) mediates cholinergic anti-inflammatory responses. However, the pathophysiological roles of AChR in periodontitis are unclear. Here, we show that activation of AChR elicits increased cytosolic Ca²⁺ ([Ca²⁺]ᵢ), transient cytotoxicity, and induction of receptor activator of nuclear factor kappa-B ligand (RANKL) expression. Intracellular Ca²⁺ mobilization in human gingival fibroblast-1 (hGF-1) cells was measured using the fluorescent Ca²⁺ indicator, fura-2/AM. Cytotoxicity and induction of gene expression were evaluated by measuring the release of glucose-6-phosphate dehydrogenase and RT-PCR. Activation of AChR in hGF-1 cells by carbachol (Cch) induced [Ca²⁺]ᵢ increase in a dose-dependent manner. Treatment with a high concentration of Cch on hGF-1 cells caused transient cytotoxicity. Notably, treatment of hGF-1 cells with Cch resulted in upregulated RANKL expression. The findings may indicate potential roles of AChR in gingival fibroblast cells in bone remodeling.
Key words
Full text:
1
Index:
WPRIM
Main subject:
Periodontitis
/
Carbachol
/
Acetylcholine
/
Gene Expression
/
Receptors, Cholinergic
/
Bone Remodeling
/
Cytosol
/
Epithelial Cells
/
Osteoprotegerin
/
Fibroblasts
Limits:
Humans
Language:
Ko
Journal:
International Journal of Oral Biology
Year:
2016
Type:
Article