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Related Concept Videos

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...

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Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
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Tumor necrosis factor-alpha modulates monocyte/macrophage apoprotein E gene expression

H Duan1, Z Li, T Mazzone

  • 1Department of Medicine, Rush Medical College, Chicago, Illinois 60612, USA.

The Journal of Clinical Investigation
|August 1, 1995
PubMed
Summary

Tumor necrosis factor-alpha (TNF α) significantly increases apolipoprotein E (apo E) mRNA in monocytes and macrophages. This regulation of apo E by TNF α influences cholesterol balance and atherosclerotic plaque development.

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Area of Science:

  • Biochemistry
  • Immunology
  • Cardiovascular Biology

Background:

  • Apolipoprotein E (apo E) plays a crucial role in cholesterol homeostasis within arterial wall cells.
  • Macrophage-derived apo E production within atherosclerotic plaques is implicated in lesion development.
  • Cytokines, such as tumor necrosis factor-alpha (TNF α), are present in human atherosclerotic lesions.

Purpose of the Study:

  • To investigate the impact of TNF α on apolipoprotein E (apo E) production in human monocytes and macrophages.
  • To elucidate the molecular mechanisms underlying TNF α-mediated regulation of apo E.

Main Methods:

  • Treatment of freshly isolated human monocytes and differentiated macrophages with TNF α.
  • Analysis of apo E mRNA abundance using quantitative methods.
  • Assessment of apo E protein synthesis.
  • Investigation of gene expression changes (c-fos, ICAM-1) and DNA synthesis.
  • Examination of TNF α effects using cell-permanent ceramide analogues and protein kinase C antagonists.
  • Studies on TNF α-induced apo E gene transcription via promoter-dependent reporter assays.

Main Results:

  • TNF α caused a 4- to 5-fold increase in apo E mRNA in freshly isolated human monocytes.
  • In differentiated macrophages, TNF α had no effect or modestly inhibited apo E mRNA expression.
  • THP1 monocytic cells exhibited a phenotype-specific response to TNF α, with increased apo E mRNA, synthesis, and stimulated apo E promoter activity.
  • TNF α treatment also induced c-fos and ICAM-1 gene expression and inhibited DNA synthesis in THP1 cells.
  • Protein kinase C antagonists, but not ceramide analogues, inhibited the TNF α effect on apo E.

Conclusions:

  • TNF α regulates apo E gene transcription, mRNA abundance, and protein synthesis in a phenotype-specific manner within monocytes/macrophages.
  • This TNF α-mediated regulation of apo E can significantly alter the apo E levels in vascular lesions.
  • The findings highlight a potential mechanism linking inflammation and lipid metabolism in atherosclerosis.