Title : Nicotine elevated intracellular Ca²⁺ in rat airway smooth muscle cells via activating and up-regulating α7-nicotinic acetylcholine receptor.

Pub. Date : 2014

PMID : 24525957






10 Functional Relationships(s)
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1 Chronic nicotine exposure increased alpha7-nAChR mRNA and protein expression, and elevated resting [Ca(2+)]i in cultured rat ASMCs. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus
2 Nicotine-induced Ca(2+) response was reversibly blocked by the alpha7-nAChR nicotinic antagonists, methyllycaconitine and alpha-bungarotoxin. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus
3 Small interfering RNA suppression of alpha7-nAChR also substantially blunted the Ca(2+) responses induced by nicotine. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus
4 CONCLUSION: These observations suggest that nicotine elevates [Ca(2+)]i in ASMCs through alpha7-nAChR-mediated signals pathways, and highlight the possibility that alpha7-nAChR can be considered as a potential target for the treatment of airway remodeling.that nicotine elevates [Ca(2+)]i in ASMCs through alpha7-nAChR-mediated signals pathways, and highlight the possibility that alpha7-nAChR can be considered as a potential target for the treatment of airway remodeling. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus
5 CONCLUSION: These observations suggest that nicotine elevates [Ca(2+)]i in ASMCs through alpha7-nAChR-mediated signals pathways, and highlight the possibility that alpha7-nAChR can be considered as a potential target for the treatment of airway remodeling.that nicotine elevates [Ca(2+)]i in ASMCs through alpha7-nAChR-mediated signals pathways, and highlight the possibility that alpha7-nAChR can be considered as a potential target for the treatment of airway remodeling. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus
6 CONCLUSION: These observations suggest that nicotine elevates [Ca(2+)]i in ASMCs through alpha7-nAChR-mediated signals pathways, and highlight the possibility that alpha7-nAChR can be considered as a potential target for the treatment of airway remodeling.that nicotine elevates [Ca(2+)]i in ASMCs through alpha7-nAChR-mediated signals pathways, and highlight the possibility that alpha7-nAChR can be considered as a potential target for the treatment of airway remodeling. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus
7 CONCLUSION: These observations suggest that nicotine elevates [Ca(2+)]i in ASMCs through alpha7-nAChR-mediated signals pathways, and highlight the possibility that alpha7-nAChR can be considered as a potential target for the treatment of airway remodeling.that nicotine elevates [Ca(2+)]i in ASMCs through alpha7-nAChR-mediated signals pathways, and highlight the possibility that alpha7-nAChR can be considered as a potential target for the treatment of airway remodeling. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus
8 CONCLUSION: These observations suggest that nicotine elevates [Ca(2+)]i in ASMCs through alpha7-nAChR-mediated signals pathways, and highlight the possibility that alpha7-nAChR can be considered as a potential target for the treatment of airway remodeling.that nicotine elevates [Ca(2+)]i in ASMCs through alpha7-nAChR-mediated signals pathways, and highlight the possibility that alpha7-nAChR can be considered as a potential target for the treatment of airway remodeling. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus
9 CONCLUSION: These observations suggest that nicotine elevates [Ca(2+)]i in ASMCs through alpha7-nAChR-mediated signals pathways, and highlight the possibility that alpha7-nAChR can be considered as a potential target for the treatment of airway remodeling.that nicotine elevates [Ca(2+)]i in ASMCs through alpha7-nAChR-mediated signals pathways, and highlight the possibility that alpha7-nAChR can be considered as a potential target for the treatment of airway remodeling. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus
10 CONCLUSION: These observations suggest that nicotine elevates [Ca(2+)]i in ASMCs through alpha7-nAChR-mediated signals pathways, and highlight the possibility that alpha7-nAChR can be considered as a potential target for the treatment of airway remodeling.that nicotine elevates [Ca(2+)]i in ASMCs through alpha7-nAChR-mediated signals pathways, and highlight the possibility that alpha7-nAChR can be considered as a potential target for the treatment of airway remodeling. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus