C‑reactive protein/oxidized low density lipoprotein/β2‑glycoprotein i complexes induce lipid accumulation and inflammatory reaction in macrophages via p38/mitogen‑activated protein kinase and nuclear factor‑κB signaling pathways

  • Authors:
    • Jie Wang
    • Mei‑Jun Feng
    • Rui Zhang
    • De‑Min Yu
    • Sai‑Jun Zhou
    • Rui Chen
    • Pei Yu
  • View Affiliations

  • Published online on: August 11, 2016     https://doi.org/10.3892/mmr.2016.5622
  • Pages: 3490-3498
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Abstract

Oxidized low-density lipoprotein (oxLDL) can bind to β2-glycoprotein I (β2GPI) and C-reactive protein (CRP) to form stable complexes, which exert certain effects in diabetic cardiovascular disease. A previous study by our group has confirmed that the resulting complexes promote atherosclerosis in diabetic BALB/c mice. The present study was designed to investigate the effects and potential mechanisms of oxLDL complexes on lipid accumulation and inflammatory reactions in RAW264.7 macrophages cultured in a hyperglycemic environment. Cultured cells were divided into seven groups, which were treated with phosphate‑buffered saline (control), CRP, β2GPI, oxLDL, CRP/oxLDL, oxLDL/β2GPI or CRP/oxLDL/β2GPI. The results revealed the formation of foam cells in the oxLDL, CRP/oxLDL, oxLDL/β2GPI as well as CRP/oxLDL/β2GPI groups. Compared with oxLDL, the three complexes induced less lipid accumulation (P<0.05) through inhibiting the expression of CD36 mRNA and promoting the expression of and ABCG1 mRNA (P<0.05 vs. oxLDL). Furthermore, the levels of inflammatory factors interleukin (IL)‑1β, IL‑6 and tumor necrosis factor‑α were elevated in the CRP/oxLDL and CRP/oxLDL/β2GPI groups (P>0.05 vs. oxLDL), and obvious effects on p38/mitogen‑activated protein kinase and nuclear factor (NF)‑κB phosphorylation were also observed in these groups (P<0.05 vs. oxLDL). These results suggested that CRP/oxLDL/βG2P1 complexes may induce lipid accumulation and inflammation in macrophages via the p38/MAPK and NF‑κB signaling pathways. However, some differences were observed between the complexes, which may be attributed to the property of each constituent; therefore, further studies are required.
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October-2016
Volume 14 Issue 4

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Wang J, Feng MJ, Zhang R, Yu DM, Zhou SJ, Chen R and Yu P: C‑reactive protein/oxidized low density lipoprotein/β2‑glycoprotein i complexes induce lipid accumulation and inflammatory reaction in macrophages via p38/mitogen‑activated protein kinase and nuclear factor‑κB signaling pathways. Mol Med Rep 14: 3490-3498, 2016
APA
Wang, J., Feng, M., Zhang, R., Yu, D., Zhou, S., Chen, R., & Yu, P. (2016). C‑reactive protein/oxidized low density lipoprotein/β2‑glycoprotein i complexes induce lipid accumulation and inflammatory reaction in macrophages via p38/mitogen‑activated protein kinase and nuclear factor‑κB signaling pathways. Molecular Medicine Reports, 14, 3490-3498. https://doi.org/10.3892/mmr.2016.5622
MLA
Wang, J., Feng, M., Zhang, R., Yu, D., Zhou, S., Chen, R., Yu, P."C‑reactive protein/oxidized low density lipoprotein/β2‑glycoprotein i complexes induce lipid accumulation and inflammatory reaction in macrophages via p38/mitogen‑activated protein kinase and nuclear factor‑κB signaling pathways". Molecular Medicine Reports 14.4 (2016): 3490-3498.
Chicago
Wang, J., Feng, M., Zhang, R., Yu, D., Zhou, S., Chen, R., Yu, P."C‑reactive protein/oxidized low density lipoprotein/β2‑glycoprotein i complexes induce lipid accumulation and inflammatory reaction in macrophages via p38/mitogen‑activated protein kinase and nuclear factor‑κB signaling pathways". Molecular Medicine Reports 14, no. 4 (2016): 3490-3498. https://doi.org/10.3892/mmr.2016.5622