Release of calcium from inositol 1,4,5-trisphosphate receptor-regulated stores by HIV-1 Tat regulates TNF-alpha production in human macrophages

J Immunol. 2000 Jun 15;164(12):6538-42. doi: 10.4049/jimmunol.164.12.6538.

Abstract

HIV-1 protein Tat is neurotoxic and increases macrophage and microglia production of TNF-alpha, a cytopathic cytokine linked to the neuropathogenesis of HIV dementia. Others have shown that intracellular calcium regulates TNF-alpha production in macrophages, and we have shown that Tat releases calcium from inositol 1,4, 5-trisphosphate (IP3) receptor-regulated stores in neurons and astrocytes. Accordingly, we tested the hypothesis that Tat-induced TNF-alpha production was dependent on the release of intracellular calcium from IP3-regulated calcium stores in primary macrophages. We found that Tat transiently and dose-dependently increased levels of intracellular calcium and that this increase was blocked by xestospongin C, pertussis toxin, and by phospholipase C and type 1 protein kinase C inhibitors but not by protein kinase A or phospholipase A2 inhibitors. Xestospongin C, BAPTA-AM, U73122, and bisindolylmalemide significantly inhibited Tat-induced TNF-alpha production. These results demonstrate that in macrophages, Tat-induced release of calcium from IP3-sensitive intracellular stores and activation of nonconventional PKC isoforms play an important role in Tat-induced TNF-alpha production.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Calcium / metabolism*
  • Calcium Channels / physiology*
  • Calcium Signaling / immunology
  • Cells, Cultured
  • Dose-Response Relationship, Immunologic
  • Estrenes / pharmacology
  • Gene Products, tat / physiology*
  • HIV-1 / physiology*
  • Humans
  • Inositol 1,4,5-Trisphosphate / metabolism
  • Inositol 1,4,5-Trisphosphate Receptors
  • Intracellular Fluid / metabolism
  • Macrophages / drug effects
  • Macrophages / immunology
  • Macrophages / metabolism*
  • Pertussis Toxin
  • Pyrrolidinones / pharmacology
  • Receptors, Cytoplasmic and Nuclear / physiology*
  • Time Factors
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / biosynthesis*
  • Type C Phospholipases / physiology
  • Virulence Factors, Bordetella / pharmacology
  • tat Gene Products, Human Immunodeficiency Virus

Substances

  • Calcium Channels
  • Estrenes
  • Gene Products, tat
  • ITPR1 protein, human
  • Inositol 1,4,5-Trisphosphate Receptors
  • Pyrrolidinones
  • Receptors, Cytoplasmic and Nuclear
  • Tumor Necrosis Factor-alpha
  • Virulence Factors, Bordetella
  • tat Gene Products, Human Immunodeficiency Virus
  • 1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione
  • Inositol 1,4,5-Trisphosphate
  • Pertussis Toxin
  • Type C Phospholipases
  • Calcium