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International Journal of Oral Biology ; : 119-123, 2016.
Artículo en Coreano | WPRIM | ID: wpr-124491

RESUMEN

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.


Asunto(s)
Humanos , Acetilcolina , Remodelación Ósea , Carbacol , Citosol , Células Epiteliales , Fibroblastos , Expresión Génica , Glucosafosfato Deshidrogenasa , Neuronas , Osteoprotegerina , Periodontitis , Receptores Colinérgicos
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