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- W2079606009 abstract "Abstract —The aim of the present study was to (1) evaluate the responsiveness of human mononuclear cells to lipoprotein lipase (LPL), as assessed by tumor necrosis factor-α (TNFα) production, during the process of differentiation of monocytes to macrophages, and (2) determine the mechanisms by which LPL exerts its effect on these cells. Treatment of human monocytes with purified endotoxin-free bovine LPL (1 μg/mL) resulted in a 161±15% increase in TNFα production over control values ( P <0.01). A further increase in TNFα production was observed after treatment of monocyte-derived macrophages (MDMs) with LPL (490±81% over control values, P <0.01). Increased TNFα mRNA expression and protein kinase C activity were also observed in LPL-treated human monocytes and MDMs. These LPL effects were abrogated by the specific protein kinase C inhibitor calphostin C (1 μmol/L). Although heparinase totally abolished LPL-induced TNFα production in human monocytes, this agent did not significantly inhibit LPL effect in human MDMs. In contrast, treatment of MDMs with chondroitinase suppressed LPL-induced TNFα production. Taken together, these data suggest that (1) differentiation of human monocytes to MDMs is associated with increased LPL-induced TNFα mRNA expression and production, (2) a protein kinase C–dependent pathway is involved in the induction of TNFα by LPL in these cells, and (3) LPL effect is mediated by cell surface proteoglycans. As MDMs secrete LPL in the vascular wall, we propose that LPL, by acting as an autocrine activator of MDM function, may contribute to the high level of TNFα found in the atheromatous lesion." @default.
- W2079606009 created "2016-06-24" @default.
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- W2079606009 date "1999-06-01" @default.
- W2079606009 modified "2023-10-01" @default.
- W2079606009 title "Differentiation of Human Monocytes to Monocyte-Derived Macrophages Is Associated With Increased Lipoprotein Lipase–Induced Tumor Necrosis Factor-α Expression and Production" @default.
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- W2079606009 doi "https://doi.org/10.1161/01.atv.19.6.1405" @default.
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