Abstract

 
 
 
 Purpose: To study the impact of cigarette smoke extract (CSE) on the migratory capacity of rat vascular smooth muscle cells (VSMCs), and the likely mechanism of action involved.
 Methods: Rat VSMCs were exposed to varying concentrations of CSE. The migration capacity of the cells was determined by Transwell migration assay and scratch test. Protein and RNA expression levels of LATS1 (large tumor suppressor kinase 1) and MOB2 (monopolar spindle-one-binder protein 2) were assayed using immunoblotting and quantitative real-time-polymerase chain reaction (qRT-PCR), respectively.
 Results: The results showed that within a certain concentration range, the migratory capacity of VSMCs increased as the concentration of CSE increased (p < 0.05). In contrast, the protein and RNA expressions of LATS1 and MOB2 were negatively correlated with CSE concentrations (p < 0.05).
 Conclusion: CSE promotes abnormal migration of rat VSMCs by inhibiting the expressions of LATS1 and MOB2 associated with Hippo signaling pathway. Thus, smoking may induce vascular remodeling and cardiovascular events via this mechanism.
 
 
 
Highlights
Coronary heart disease (CHD) is a primary disease which seriously threatens human health and causes mortality worldwide
It has been shown that vascular remodeling is a shared pathophysiological process which leads to cardiovascular diseases (CVDs) such as coronary heart disease, in-stent re-stenosis following percutaneous coronary
There was a marked increase in the population of vascular smooth muscle cells (VSMCs) that moved to the lower compartment at each cigarette smoke extract (CSE) concentration group, relative to negative control value
Summary
Coronary heart disease (CHD) is a primary disease which seriously threatens human health and causes mortality worldwide. With improvements in living standards, the incidence of CHD has noticeably increased. It is generally believed that smoking contributes significantly to incidents of CHD. The global report of the World Health Organization (WHO) on Prevalence of Tobacco Use (2000 - 2025) stated that smoking and passive smoking are important factors that predispose to severe cardiovascular diseases (CVDs). About 3 million CVD patients annually die because of smoking or passive smoking [1]. It has been shown that vascular remodeling is a shared pathophysiological process which leads to CVDs such as coronary heart disease, in-stent re-stenosis following percutaneous coronary
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