Acute cigarette smoke or extract exposure rapidly activates TRPA1-mediated calcium influx in primary human airway smooth muscle cells.

ABSTRACT: Tobacco smoking is the largest risk factor for developing chronic obstructive pulmonary disease (COPD), and is associated with hyperresponsiveness of airway smooth muscle (ASM). Chronic exposure to cigarette smoke (CS) leads to airway inflammation and remodelling. However, the direct effect of gaseous CS or CS extract (CSE) on human airway smooth muscle cell (hASMC) function remains poorly understood. This study investigated the acute effect of CS/CSE on calcium homeostasis, a key regulator of ASM physiology and pathophysiology. Primary hASMC were isolated from non-smoking donor lungs, and subjected to Ca²⁺ imaging studies. We found that both CS, and CSE, rapidly elevated cytosolic Ca²⁺ in hASMC through stimulation of plasmalemmal Ca²⁺ influx, but excluded

SUBMITTER: Lin J 

PROVIDER: S-EPMC8100124 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature