Se-methylselenocysteine enhances PMA-mediated CD11c expression via phospholipase D1 activation in U937 cells

Tae Jin Lee, Young Ho Kim, Do Sik Min, Jong Wook Park, Taeg Kyu Kwon

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

CD11c/CD18 is expressed primarily on myeloid cells, where its expression is regulated both during differentiation and during monocyte maturation into tissue macrophages, and is also a receptor for fibrinogen and lipopolysaccharide (LPS). We focused on the molecular mechanisms leading to the activation of CD11c expression in differentiating U937 cells. During phorbol myristate acetate (PMA)-induced differentiation of U937 cells, we found that the mRNA expression of CD11c was increased. Se-methylselenocysteine (Se-MSC) potentiated up-regulation of CD11c expression and its promoter activity and increased PLD1 activity without affecting the level of PLD1 protein in PMA-treated cells. To examine the regulation mechanism of PMA and Se-MSC on CD11c gene expression through the activation of PLD1, we analyzed changes in the CD11c mRNA level and the promoter activity following treatment of a selective PLD inhibitor n-butanol. The combinatory effect of PMA and Se-MSC on CD11c gene expression was abolished by n-butanol in a dose-dependent manner. Further, introduction of PLD1 gene into U937 cells increased CD11c mRNA expression and activated CD11c promoter activity in a dose-dependent manner. These results showed that Se-MSC increased PMA-induced CD11c expression through the activation of PLD1 signaling pathway. To our knowledge, this is the first report that expression of the CD11c gene is regulated by PLD1 and is enhanced by Se-MSC during PMA-induced U937 differentiation.

Original languageEnglish
Pages (from-to)369-376
Number of pages8
JournalImmunobiology
Volume211
Issue number5
DOIs
Publication statusPublished - 2006 Jun 16

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U937 Cells
Tetradecanoylphorbol Acetate
1-Butanol
Gene Expression
Messenger RNA
Fibrinogen Receptors
CD14 Antigens
Myeloid Cells
phospholipase D1
selenomethylselenocysteine
Monocytes
Up-Regulation
Macrophages
Genes
Proteins

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Hematology

Cite this

Lee, Tae Jin ; Kim, Young Ho ; Min, Do Sik ; Park, Jong Wook ; Kwon, Taeg Kyu. / Se-methylselenocysteine enhances PMA-mediated CD11c expression via phospholipase D1 activation in U937 cells. In: Immunobiology. 2006 ; Vol. 211, No. 5. pp. 369-376.
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Se-methylselenocysteine enhances PMA-mediated CD11c expression via phospholipase D1 activation in U937 cells. / Lee, Tae Jin; Kim, Young Ho; Min, Do Sik; Park, Jong Wook; Kwon, Taeg Kyu.

In: Immunobiology, Vol. 211, No. 5, 16.06.2006, p. 369-376.

Research output: Contribution to journalArticle

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T1 - Se-methylselenocysteine enhances PMA-mediated CD11c expression via phospholipase D1 activation in U937 cells

AU - Lee, Tae Jin

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AB - CD11c/CD18 is expressed primarily on myeloid cells, where its expression is regulated both during differentiation and during monocyte maturation into tissue macrophages, and is also a receptor for fibrinogen and lipopolysaccharide (LPS). We focused on the molecular mechanisms leading to the activation of CD11c expression in differentiating U937 cells. During phorbol myristate acetate (PMA)-induced differentiation of U937 cells, we found that the mRNA expression of CD11c was increased. Se-methylselenocysteine (Se-MSC) potentiated up-regulation of CD11c expression and its promoter activity and increased PLD1 activity without affecting the level of PLD1 protein in PMA-treated cells. To examine the regulation mechanism of PMA and Se-MSC on CD11c gene expression through the activation of PLD1, we analyzed changes in the CD11c mRNA level and the promoter activity following treatment of a selective PLD inhibitor n-butanol. The combinatory effect of PMA and Se-MSC on CD11c gene expression was abolished by n-butanol in a dose-dependent manner. Further, introduction of PLD1 gene into U937 cells increased CD11c mRNA expression and activated CD11c promoter activity in a dose-dependent manner. These results showed that Se-MSC increased PMA-induced CD11c expression through the activation of PLD1 signaling pathway. To our knowledge, this is the first report that expression of the CD11c gene is regulated by PLD1 and is enhanced by Se-MSC during PMA-induced U937 differentiation.

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