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Triglyceride Regulates the Expression of M1 and M2 Macrophage-specific Markers in THP-1 Monocytes

  • Kim, Hyun-Kyung (Department of Biomedical Laboratory Science, College of Health Sciences, Yonsei University) ;
  • Kim, Sung Hoon (Department of Biomedical Laboratory Science, College of Health Sciences, Yonsei University) ;
  • Kang, Yeo Wool (Department of Biomedical Laboratory Science, College of Health Sciences, Yonsei University) ;
  • Kim, Bohee (Department of Biomedical Laboratory Science, College of Health Sciences, Yonsei University) ;
  • Rhee, Ki-Jong (Department of Biomedical Laboratory Science, College of Health Sciences, Yonsei University) ;
  • Kim, Yoon Suk (Department of Biomedical Laboratory Science, College of Health Sciences, Yonsei University)
  • Received : 2016.10.28
  • Accepted : 2016.11.14
  • Published : 2016.12.31

Abstract

Hypertriglyceridemia induces atherosclerosis and accordingly is a major causative factor in cardiovascular diseases. Macrophages that develop into foam cells are a crucial component in the development of atherosclerosis. Monocytes can be differentiated into M1 or M2 macrophages. M1 macrophages promote inflammatory responses, whereas M2 macrophages exhibit anti-inflammatory activity. Recently, we found that triglyceride (TG)-treated THP-1 monocytes express a variety of macrophage-specific surface markers, indicating that TG treatment could trigger the differentiation of monocytes into macrophages. In this study, we investigated whether TG-induced macrophages express the M1 or the M2 macrophage phenotype. THP-1 cells were treated with various concentrations of TG for different times and the expression of M1- and M2-specific markers was evaluated by RT-PCR. We found increased expression of M1 markers (CD40, CD80, and CD86) in TG-treated THP-1 cells in a TG dose- and time-dependent manner. The expression of M2 markers (CD163, CD200R, and CD206) showed variable responses to TG treatment. Taken together, our results indicate that TG treatment triggers the differentiation of monocytes into M1 macrophages, rather than into M2 macrophages, suggesting that TG contributes to pro-inflammatory responses.

Keywords

References

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