Lipopolysaccharide augments the uptake of oxidized LDL by up-regulating lectin-like oxidized LDL receptor-1 in macrophages

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• 作者：Ekhtear Hossain (1)
  Akinobu Ota (1) (3)
  Sivasundaram Karnan (1)
  Miyuki Takahashi (1) (2)
  Shahnewaj B. Mannan (1)
  Hiroyuki Konishi (1)
  Yoshitaka Hosokawa (1)
  
  1. Department of Biochemistry ; Aichi Medical University School of Medicine ; Nagakute ; Aichi ; Japan
  3. Department of Biochemistry ; Aichi Medical University School of Medicine ; 1-1 Yazakokarimata ; Building #2 ; Room 362 ; Nagakute ; Aichi ; 480-1195 ; Japan
  2. Division of Hematology ; Department of Internal Medicine ; Aichi Medical University School of Medicine ; Nagakute ; Aichi ; Japan
  
• 关键词：LPS ; LOX ; 1 ; Atherosclerosis ; Erk1/2 ; Molecular biology
• 刊名：Molecular and Cellular Biochemistry
• 出版年：2015
• 出版时间：February 2015
• 年：2015
• 卷：400
• 期：1-2
• 页码：29-40
• 全文大小：3,021 KB
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• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Life Sciences
  Biochemistry
  Medical Biochemistry
  Oncology
  Cardiology
  
• 出版者：Springer Netherlands
• ISSN：1573-4919

文摘

There is a growing body of evidence supporting an intimate association of immune activation with the pathogenesis of cardiovascular diseases, including atherosclerosis. Uptake of oxidized low-density lipoprotein (oxLDL) through scavenging receptors promotes the formation of mature lipid-laden macrophages, which subsequently leads to exacerbation of regional inflammation and atherosclerotic plaque formation. In this study, we first examined changes in the mRNA level of the lectin-like oxLDL receptor-1 (LOX-1) in the mouse macrophage cell line RAW264.7 and the human PMA-induced macrophage cell line THP-1 after LPS stimulation. LPS significantly up-regulated LOX-1 mRNA in RAW264.7 cells; LOX-1 cell-surface protein expression was also increased. Flow cytometry and fluorescence microscopy analyses showed that cellular uptake of fluorescence (Dil)-labeled oxLDL was significantly augmented with LPS stimulation. The augmented uptake of Dil-oxLDL was almost completely abrogated by treatment with an anti-LOX-1 antibody. Of note, knockdown of Erk1/2 resulted in a significant reduction of LPS-induced LOX-1 up-regulation. Treatment with U0126, a specific inhibitor of MEK, significantly suppressed LPS-induced expression of LOX-1 at both the mRNA and protein levels. Furthermore, LOX-1 promoter activity was significantly augmented by LPS stimulation; this augmentation was prevented by U0126 treatment. Similar results were also observed in human PMA-induced THP-1 macrophages. Taken together, our results indicate that LPS up-regulates LOX-1, at least in part through activation of the Erk1/2 signaling pathway, followed by augmented cellular oxLDL uptake, thus highlighting a critical role of TLR4-mediated aberrant LOX-1 signaling in the pathogenesis of atherosclerosis.