Peripheral benzodiazepine receptor modulation with phagocyte differentiation

Biochem Pharmacol. 1993 Aug 3;46(3):551-4. doi: 10.1016/0006-2952(93)90535-5.

Abstract

Peripheral benzodiazepine receptor (PBR) was found to be less expressed in the immature phagocytic HL-60 and U-937 cell lines than in the more mature monocytic THP-1 cell line. Cell differentiation by several agents induced a strong enhancement of PBR density on these three phagocytic cell lines but not on the lymphocytic CEM cell line. Detailed analysis of phorbol 12-myristate 13-acetate-treated THP-1 cells showed an increased PBR expression and the rise came along with an increase of CD11a and CD11b antigens and a secretion of macrophagic cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta and IL-8. Quantitation of mRNA using polymerase chain reaction (PCR)-based technique showed that overexpression of PBR did not parallel mRNA expression, indicating a gene-independent regulation. These results suggest that PBR predominance on phagocytic cells could be related to maturation process.

Publication types

  • Comparative Study

MeSH terms

  • Antigens, CD / analysis
  • Binding Sites / drug effects
  • Cell Differentiation
  • Cell Line
  • Dimethyl Sulfoxide / pharmacology
  • Humans
  • Interferon-gamma / pharmacology
  • Interleukin-1 / analysis
  • Interleukin-8 / analysis
  • Phagocytes / drug effects
  • Phagocytes / metabolism*
  • RNA, Messenger / analysis
  • Receptors, GABA-A / genetics
  • Receptors, GABA-A / immunology
  • Receptors, GABA-A / metabolism*
  • Tetradecanoylphorbol Acetate / pharmacology
  • Tumor Necrosis Factor-alpha / analysis

Substances

  • Antigens, CD
  • Interleukin-1
  • Interleukin-8
  • RNA, Messenger
  • Receptors, GABA-A
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma
  • Tetradecanoylphorbol Acetate
  • Dimethyl Sulfoxide