【bio-news】氧化低密度脂蛋白通过氧化应激增加骨桥蛋白表达
发布于 2010-10-22 · 浏览 1798 · IP 山东山东
这个帖子发布于 14 年零 199 天前，其中的信息可能已发生改变或有所发展。
Oxidized low-density lipoprotein increases osteopontin expression by generation of oxidative stress.
Mazière C, Gomila C, Mazière JC.
Biochemistry Laboratory, CHU Nord, Amiens F-80000, France. maziere.cecile@chu-amiens.fr
Abstract
Osteopontin (OPN) is an important mediator of inflammation and is involved in the generation of atherosclerotic lesions. Oxidized LDL (OxLDL) increased the intracellular and secreted levels of OPN in rat smooth muscle cells in a dose- and time-dependent manner. Experiments with kinase inhibitors demonstrated that this effect was mediated by ERK and JNK, but not p38. OxLDL induced oxidative stress, measured by the intracellular levels of reactive oxygen species (ROS) and lipid peroxidation products. The increase in OPN levels was reproduced by the lipid extract of the particle and prevented by the antioxidant vitamin E. Furthermore, ROS generated by UVA irradiation or treatment with pro-oxidant compounds such as buthionine sulfoximine or H(2)O(2) also enhanced intracellular and secreted OPN. Finally, OxLDL also augmented OPN levels in other cell types such as fibroblasts, keratinocytes, and endothelial cells. This work demonstrates the role of OxLDL in the expression of the OPN gene and further highlights the role of oxidative stress in the regulation of this cytokine. This might be related to the proinflammatory effects of OxLDL in the initiation and progression of atherosclerotic plaque.
Copyright 2010 Elsevier Inc. All rights reserved.
Mazière C, Gomila C, Mazière JC.
Biochemistry Laboratory, CHU Nord, Amiens F-80000, France. maziere.cecile@chu-amiens.fr
Abstract
Osteopontin (OPN) is an important mediator of inflammation and is involved in the generation of atherosclerotic lesions. Oxidized LDL (OxLDL) increased the intracellular and secreted levels of OPN in rat smooth muscle cells in a dose- and time-dependent manner. Experiments with kinase inhibitors demonstrated that this effect was mediated by ERK and JNK, but not p38. OxLDL induced oxidative stress, measured by the intracellular levels of reactive oxygen species (ROS) and lipid peroxidation products. The increase in OPN levels was reproduced by the lipid extract of the particle and prevented by the antioxidant vitamin E. Furthermore, ROS generated by UVA irradiation or treatment with pro-oxidant compounds such as buthionine sulfoximine or H(2)O(2) also enhanced intracellular and secreted OPN. Finally, OxLDL also augmented OPN levels in other cell types such as fibroblasts, keratinocytes, and endothelial cells. This work demonstrates the role of OxLDL in the expression of the OPN gene and further highlights the role of oxidative stress in the regulation of this cytokine. This might be related to the proinflammatory effects of OxLDL in the initiation and progression of atherosclerotic plaque.
Copyright 2010 Elsevier Inc. All rights reserved.
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