Nicotine Induces Pro-inflammatory Response in Aortic Vascular Smooth Muscle Cells Through a NFκB/Osteopontin Amplification Loop-Dependent Pathway

Nicotine has anti- and pro-inflammatory properties in various cells. Its role in aortic vascular smooth muscle cells (VSMC) was explored. Human aortic VSMC were cultured. After nicotine (1.0 mu M) and/or pyrrolidinedithiocarbamic acid (PDTC, 50 mu M) treatment, the activation of nuclear factor kappa B (NF kappa B) was investigated. The levels of pro-inflammatory cytokines, osteopontin (OPN), interleukin-6 (IL-6), and monocyte chemoattractant protein 1 (MCP-1) were also assessed. After OPN was downregulated by small interfering RNA (siRNA) transfection, the pro-inflammatory effect was reassessed. We found that NF kappa B was activated after nicotine administration. Nicotine upregulated OPN, IL-6, and MCP-1 expressions, and this effect attenuated after PDTC pretreatment. RNAi knocked down the OPN expression in nicotine-treated cells and abolished its pro-inflammatory effects. We concluded that nicotine induces a pro-inflammatory response in VSMC through a NF kappa B/osteopontin amplification loop-dependent pathway.