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Chronic obstructive pulmonary disease (COPD) is characterized by airway remodeling with airway smooth muscle (ASM) hypertrophy and hyperplasia. Since tobacco use is the key risk factor for the development of COPD and intracellular Ca(2+) concentration ([Ca(2+)]i) plays a major role in both cell proliferation and differentiation, we hypothesized that nicotinic acetylcholine receptor (nAChR) activation plays a role in the elevation of [Ca(2+)]i in airway smooth muscle cells (ASMCs).

Nicotine Elevated Intracellular Ca2+in Rat Airway Smooth Muscle Cells via Activating and Up-Regulating a7-Nicotinic Acetylcholine Receptor

Nicotine Elevated Intracellular Ca²⁺in Rat Airway Smooth Muscle Cells via Activating and Up-Regulating a7-Nicotinic Acetylcholine Receptor