Nicotine Elevated Intracellular Ca2+in Rat Airway Smooth Muscle Cells via Activating and Up-Regulating a7-Nicotinic Acetylcholine Receptor
Author(s) -
YongLiang Jiang,
Aiguo Dai,
Yumin Zhou,
Gongyong Peng,
Guoping Hu,
Bing Li,
James S.K. Sham,
Pixin Ran
Publication year - 2014
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000356678
Subject(s) - methyllycaconitine , nicotine , nicotinic acetylcholine receptor , nicotinic agonist , acetylcholine , intracellular , chemistry , medicine , endocrinology , acetylcholine receptor , microbiology and biotechnology , receptor , pharmacology , biology
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).
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