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  • Toll-like Receptor 4 Stimulates Gene Expression via Smad2 Linker Region Phosphorylation in Vascular Smooth Muscle Cells

    Author(s)
    Afroz, Rizwana
    Zhou, Ying
    Little, Peter J
    Xu, Suowen
    Mohamed, Raafat
    Stow, Jennifer
    Kamato, Danielle
    Griffith University Author(s)
    Afroz, Rizwana
    Kamato, Danielle
    Year published
    2020
    Metadata
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    Abstract
    Atherosclerosis begins in the vessel wall with the retention of low density lipoproteins to modified proteoglycans with hyperelongated glycosaminoglycan (GAG) chains. Bacterial infections produce endotoxins such as lipopolysaccharide that exacerbate the outcome of atherosclerosis by generating a heightened state of inflammation. Lipopolysaccharide (LPS) via its toll-like receptor (TLR) is well-known for its role in mediating an inflammatory response in the body. Emerging evidence demonstrates that TLRs are involved in regulating vascular functions. In this study we sought to investigate the role of LPS in proteoglycan ...
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    Atherosclerosis begins in the vessel wall with the retention of low density lipoproteins to modified proteoglycans with hyperelongated glycosaminoglycan (GAG) chains. Bacterial infections produce endotoxins such as lipopolysaccharide that exacerbate the outcome of atherosclerosis by generating a heightened state of inflammation. Lipopolysaccharide (LPS) via its toll-like receptor (TLR) is well-known for its role in mediating an inflammatory response in the body. Emerging evidence demonstrates that TLRs are involved in regulating vascular functions. In this study we sought to investigate the role of LPS in proteoglycan modification and GAG chain elongation, and we hypothesize that LPS will signal via Smad2 dependent pathways to regulate GAG chain elongation. The in vitro model used human aortic vascular smooth muscle cells. GAG gene expression was assessed by quantitative real-time polymerase chain reaction. Western blotting was performed using whole-cell protein lysates to assess the signaling pathway. LPS via TLR4 stimulates the expression of GAG synthesizing enzymes to an equal extent to traditional cardiovascular agonists. LPS phosphorylates the Smad2 linker region via TAK-1/MAPK dependent pathways which correlated with genes associated with GAG chain initiation and elongation. The well-characterized role of LPS in inflammation and our data on GAG gene expression demonstrates that GAG chain elongation is the earliest marker of the inflammatory cascade in atherosclerosis development.
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    Journal Title
    ACS Pharmacology & Translational Science
    Volume
    3
    Issue
    3
    DOI
    https://doi.org/10.1021/acsptsci.9b00113
    Subject
    Pharmacology and pharmaceutical sciences
    Publication URI
    http://hdl.handle.net/10072/412451
    Collection
    • Journal articles

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