Expression of the apolipoprotein C-II gene during myelomonocytic differentiation of human leukemic cells

J Leukoc Biol. 2001 Apr;69(4):645-50.

Abstract

Apolipoprotein C-II (apoC-II), which is known to activate lipoprotein lipase (LPL), was identified by ordered differential display (ODD)-polymerase chain reaction (PCR) as a cDNA fragment exhibiting a distinct increase in expression during 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced differentiation of promonocytic U937 cells into monocytes and macrophages. The amount of apoC-II mRNA expression detectable in U937 cells significantly increased and reached a maximum 24-48 h after treatment with 32 nM TPA. apoC-II mRNA was also detected in monocytic THP-1 cells but was not detected in promyelocytic HL-60 cells. In healthy human tissues, the most significant expression of apoC-II mRNA was in the liver. Although apoC-II mRNA expression was markedly up-regulated during the induced differentiation of HL-60 cells into monocytes and macrophages with 32 nM TPA, such expression was not induced during the differentiation of HL-60 cells into granulocytes with 1.25% dimethyl sulfoxide. These results suggest that human apoC-II expression is induced at the transcription level during myelomonocytic differentiation and may confer an important role to macrophages involved in normal lipid metabolism and atherosclerosis.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells / drug effects
  • 3T3 Cells / metabolism
  • Animals
  • Apolipoprotein C-II
  • Apolipoproteins C / biosynthesis*
  • Apolipoproteins C / genetics
  • Carcinoma / pathology
  • Cell Differentiation
  • Cyclin A / biosynthesis
  • Cyclin A / genetics
  • DNA, Complementary / genetics
  • Dimethyl Sulfoxide / pharmacology
  • Enzyme Activation
  • Gene Expression Profiling
  • Gene Expression Regulation, Leukemic / drug effects*
  • Granulocytes / cytology
  • Granulocytes / metabolism
  • HL-60 Cells / cytology
  • HL-60 Cells / drug effects*
  • HL-60 Cells / metabolism
  • Hematologic Neoplasms / pathology
  • Humans
  • Intestinal Mucosa / metabolism
  • Jurkat Cells / drug effects
  • Jurkat Cells / metabolism
  • Kinesins / biosynthesis
  • Kinesins / genetics
  • Lipid Metabolism
  • Lipoprotein Lipase / metabolism
  • Liver / metabolism
  • Macrophages / cytology
  • Macrophages / metabolism
  • Mice
  • Monocytes / cytology
  • Monocytes / metabolism*
  • Myeloid Cells / drug effects
  • Myeloid Cells / metabolism
  • Neoplasm Proteins / biosynthesis*
  • Neoplasm Proteins / genetics
  • Polymerase Chain Reaction
  • RNA, Messenger / biosynthesis
  • Subtraction Technique
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcription, Genetic / drug effects
  • Tumor Cells, Cultured / drug effects
  • Tumor Cells, Cultured / metabolism
  • U937 Cells / cytology
  • U937 Cells / drug effects*
  • U937 Cells / metabolism

Substances

  • Apolipoprotein C-II
  • Apolipoproteins C
  • Cyclin A
  • DNA, Complementary
  • KIF2C protein, human
  • Neoplasm Proteins
  • RNA, Messenger
  • Lipoprotein Lipase
  • Kinesins
  • Tetradecanoylphorbol Acetate
  • Dimethyl Sulfoxide