Lipopolysaccharide regulates toll-like receptor 4 expression in human aortic smooth muscle cells

Authors

  • Hongli Li,

    1. Department of Cardiology, Shanghai Jiaotong University Affiliated First People's Hospital, 85 Wujin Road, Shanghai 200080, PR China
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  • Ying He,

    1. Department of Medical Genetics, Second Military Medical University, 800 Xiangyin Road, Shanghai 200433, PR China
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    • Contributed equally to the first author.

  • Jianjun Zhang,

    1. Department of Cardiology, Shanghai Jiaotong University Affiliated First People's Hospital, 85 Wujin Road, Shanghai 200080, PR China
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  • Shuhan Sun,

    1. Department of Medical Genetics, Second Military Medical University, 800 Xiangyin Road, Shanghai 200433, PR China
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    • Contributed equally to corresponding author.

  • Baogui Sun

    Corresponding author
    1. Department of Cardiology, Shanghai Jiaotong University Affiliated First People's Hospital, 85 Wujin Road, Shanghai 200080, PR China
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Corresponding author. Tel.: +86 21 6324 0090 3052; fax: +86 21 6324 0825. bg_sun@yahoo.com

Abstract

Lipopolysaccharide (LPS) is a potent activator of cells of the immune and inflammatory systems, including macrophages, monocytes, and endothelial cells (EC). Toll-like receptor 4 (TLR4) has been identified as the primary receptor for LPS. Vascular smooth muscle cells (VSMCs) likely contribute significantly to the inflammation induced by low-level LPS in patients who are at risk for atherosclerosis. Previous study indicated that functional TLR4 was present in VSMCs. However, it remains unclear whether low levels of commercial LPS preparations can affect TLR4 expression in early stage. Here Real-time quantitative PCR analysis was used to detect TLR4 mRNA expression; Immunofluorescence, Western blot analysis and flow cytometery were used to examine TLR4 protein expression. It was shown that TLR4 was present in Human Aortic Smooth Muscle Cells (HASMCs). LPS can up-regulate TLR4 mRNA and protein expression in HASMCs in dose- and time-dependant manner. These data indicate that LPS regulate TLR4 expression in HASMCs.

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