Activation of acetylcholine receptor elicits intracellular Ca2+ mobilization, transient cytotoxicity, and induction of RANKL expression.
10.11620/IJOB.2016.41.3.119
- Author:
Seong Jong HEO
1
;
Min Seuk KIM
Author Information
1. Department of Oral Physiology, and Institute of Biomaterial-Implant, School of Dentistry, Wonkwang University, Iksan 54538, Republic of Korea. happy1487@wku.ac.kr
- Publication Type:Original Article
- Keywords:
acetylcholine receptor;
gingival fibroblast;
intracellular Ca²⁺ mobilization;
RANKL;
Osteoprotegerin
- MeSH:
Acetylcholine*;
Bone Remodeling;
Carbachol;
Cytosol;
Epithelial Cells;
Fibroblasts;
Gene Expression;
Glucosephosphate Dehydrogenase;
Humans;
Neurons;
Osteoprotegerin;
Periodontitis;
Receptors, Cholinergic
- From:International Journal of Oral Biology
2016;41(3):119-123
- CountryRepublic of Korea
- Language:Korean
-
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.
