Smooth Muscle Cell Phenotypic Switch Induced by Cigarette Smoke Condensate

Cigarette smoke is a risk factor for inflammatory diseases, such as atherosclerosis. Tobacco smoke interacts with inflammatory cytokines to produce endothelial dysfunction and induces pro-inflammatory and pro-atherosclerotic effects in vascular tissue. Smooth muscle cells (SMCs) are present in the media of human arteries, and are considered protective against atherosclerotic plaque destabilization. Contractile SMCs are the most prominent cell type in the healthy vessel wall. SMCs are not terminally differentiated, and retain the ability to undergo a phenotypic switch from a contractile to a dedifferentiated synthetic state to express inflammatory markers and a phagocytic activity in response to environmental cues. The aim of our study was to evaluate the effects in human SMCs of lipophilic component from cigarette smoke condensate (CSC) and of hydrophilic components of Electronic-cigarette, Tobacco heating products, or cigarette smoke.