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Inflammation. 2012 Feb;35(1):342-9. doi: 10.1007/s10753-011-9324-6.

Nicotine induces pro-inflammatory response in aortic vascular smooth muscle cells through a NFκB/osteopontin amplification loop-dependent pathway.

Author information

1
Department of Cardiovascular Surgery, RenJi Hospital of Shanghai Jiaotong University, Shanghai, 200127, People's Republic of China.

Abstract

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 μM) and/or pyrrolidinedithiocarbamic acid (PDTC, 50 μM) treatment, the activation of nuclear factor κB (NFκB) 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 NFκB 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 NFκB/osteopontin amplification loop-dependent pathway.

PMID:
21494800
DOI:
10.1007/s10753-011-9324-6
[Indexed for MEDLINE]

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