Triglyceride enhances susceptibility to TNF-α-induced cell death in THP-1 cells

Jaewon Lim, Yoon Suk Kim, Sung Hoon Kim, Yoonjung Cho, Min Ho Lee, Byung Chul Jung, Dongju Jung, Kijong Rhee

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Monocytes and macrophages play a major role in atherosclerosis development. Previously, we found that triglyceride (TG) promoted cell death of PMA-differentiated THP-1 macrophages. In this study, we compared the responsiveness of THP-1 monocytes and PMA-differentiated THP-1 macrophages to TNF-α-induced cell death. We found that, whereas THP-1 monocytes were TNF-α-resistant, THP-1 macrophages were sensitive to TNF-α-induced cell death. THP-1 monocytes treated with TG underwent cell death beginning at 24 h and addition of TNF-α further increased cell death. Based on these observations, we hypothesized that TG-induced differentiation of THP-1 monocytes into THP-1 macrophages, subsequently allowing sensitivity to TNF-α. To determine if TG could induce differentiation of THP-1 monocytes into THP-1 macrophages, we examined the mRNA expression levels of the macrophage-specific markers, CD11b, CD18, CD36 and CD68, by RT-PCR analysis. Our results show that expression of CD11b, CD36 and CD68 increased in TG-treated THP-1 monocytes in a dose- and time-dependent manner; furthermore, TNF-α expression was upregulated in TG-treated THP-1 monocytes. We have concluded that TG induces differentiation of THP-1 monocytes into macrophages concomitant with the production of TNF-α and increased sensitivity to TNF-α-dependent cell death.

Original languageEnglish
Pages (from-to)87-93
Number of pages7
JournalGenes and Genomics
Volume36
Issue number1
DOIs
Publication statusPublished - 2014 Jan 1

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Macrophages
Cell death
Monocytes
Triglycerides
Cell Death
Atherosclerosis
Messenger RNA
Polymerase Chain Reaction

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Genetics

Cite this

Lim, Jaewon ; Kim, Yoon Suk ; Kim, Sung Hoon ; Cho, Yoonjung ; Lee, Min Ho ; Jung, Byung Chul ; Jung, Dongju ; Rhee, Kijong. / Triglyceride enhances susceptibility to TNF-α-induced cell death in THP-1 cells. In: Genes and Genomics. 2014 ; Vol. 36, No. 1. pp. 87-93.
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abstract = "Monocytes and macrophages play a major role in atherosclerosis development. Previously, we found that triglyceride (TG) promoted cell death of PMA-differentiated THP-1 macrophages. In this study, we compared the responsiveness of THP-1 monocytes and PMA-differentiated THP-1 macrophages to TNF-α-induced cell death. We found that, whereas THP-1 monocytes were TNF-α-resistant, THP-1 macrophages were sensitive to TNF-α-induced cell death. THP-1 monocytes treated with TG underwent cell death beginning at 24 h and addition of TNF-α further increased cell death. Based on these observations, we hypothesized that TG-induced differentiation of THP-1 monocytes into THP-1 macrophages, subsequently allowing sensitivity to TNF-α. To determine if TG could induce differentiation of THP-1 monocytes into THP-1 macrophages, we examined the mRNA expression levels of the macrophage-specific markers, CD11b, CD18, CD36 and CD68, by RT-PCR analysis. Our results show that expression of CD11b, CD36 and CD68 increased in TG-treated THP-1 monocytes in a dose- and time-dependent manner; furthermore, TNF-α expression was upregulated in TG-treated THP-1 monocytes. We have concluded that TG induces differentiation of THP-1 monocytes into macrophages concomitant with the production of TNF-α and increased sensitivity to TNF-α-dependent cell death.",
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Lim, J, Kim, YS, Kim, SH, Cho, Y, Lee, MH, Jung, BC, Jung, D & Rhee, K 2014, 'Triglyceride enhances susceptibility to TNF-α-induced cell death in THP-1 cells', Genes and Genomics, vol. 36, no. 1, pp. 87-93. https://doi.org/10.1007/s13258-013-0144-y

Triglyceride enhances susceptibility to TNF-α-induced cell death in THP-1 cells. / Lim, Jaewon; Kim, Yoon Suk; Kim, Sung Hoon; Cho, Yoonjung; Lee, Min Ho; Jung, Byung Chul; Jung, Dongju; Rhee, Kijong.

In: Genes and Genomics, Vol. 36, No. 1, 01.01.2014, p. 87-93.

Research output: Contribution to journalArticle

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