Activation of acetylcholine receptor elicits intracellular Ca2+ mobilization, transient cytotoxicity, and induction of RANKL expression

서지정보

· 발행기관 : 대한구강생물학회
· 수록지 정보 : International Journal of Oral Biology / 41권 / 3호
· 저자명 : Seong-Jong Heo, Min Seuk Kim

목차

서 론
실험방법 및 실험재료
세포 배양 및 시약
세포독성 실험
RT-PCR 및 PCR
통계학적 유의성 검사
결 과
Cch 자극 정도에 따른 hGF-1 세포 내 [Ca2+]i증가
고농도 Cch 자극에 따른 hGF-1 세포 세포독성 확인
고농도 Cch 자극에 의한 hGF-1 세포 내 골 재형성 관련 유전자 발현
고 찰
References

영어초록

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.

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