Prevention of NF-kappaB activation in vivo by a cell-permeable NF-kappaB inhibitor peptide

Am J Physiol Lung Cell Mol Physiol. 2005 Oct;289(4):L536-44. doi: 10.1152/ajplung.00164.2005. Epub 2005 Jun 10.

Abstract

The NF-kappaB/Rel transcription factor family plays a central role in coordinating the expression of a variety of genes that regulate stress responses, immune cell activation, apoptosis, proliferation, differentiation, and oncogenic transformation. Interventions that target the NF-kappaB pathway may be therapeutic for a variety of pathologies, especially immune/inflammatory diseases. Using membrane translocating sequence (MTS) technology, we developed a cell-permeable dominant inhibitor of NF-kappaB activation, termed IkappaBalpha-(DeltaN)-MTS. This molecule contains a 12-amino acid MTS motif attached to the COOH-terminal region of a nondegradable inhibitor protein [IkappaBalpha-(DeltaN)]. The recombinant protein enters cells and localizes in the cytoplasm. Delivery of the IkappaBalpha-(DeltaN)-MTS to cell lines and primary cells inhibited nuclear translocation of NF-kappaB proteins induced by cell activation. The protein also effectively inhibited NF-kappaB activation in vivo in two different animal models: NF-kappaB activation in response to skin wounding in mice and NF-kappaB activation in lungs after endotoxin treatment in sheep. Inhibition of NF-kappaB by the IkappaBalpha-(DeltaN)-MTS in the endotoxin model attenuated physiological responses to endotoxemia. These data demonstrate that activation of NF-kappaB can be inhibited using a recombinant protein designed to penetrate into cells. This technology may provide a new approach to NF-kappaB pathway-targeted therapies.

Publication types

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

MeSH terms

  • Animals
  • Cell Division / immunology
  • Cell Membrane Permeability
  • Drug Delivery Systems
  • Endotoxemia / drug therapy
  • Endotoxemia / immunology
  • Gene Expression
  • Humans
  • I-kappa B Proteins / genetics
  • I-kappa B Proteins / pharmacokinetics*
  • Lung Diseases / drug therapy*
  • Lung Diseases / immunology
  • Mice
  • Mice, Inbred C57BL
  • NF-KappaB Inhibitor alpha
  • NF-kappa B / antagonists & inhibitors*
  • NF-kappa B / metabolism*
  • NIH 3T3 Cells
  • Recombinant Fusion Proteins / genetics
  • Recombinant Fusion Proteins / pharmacokinetics*
  • Sheep
  • T-Lymphocytes / drug effects
  • Thymus Gland / cytology

Substances

  • I-kappa B Proteins
  • NF-kappa B
  • NFKBIA protein, human
  • Nfkbia protein, mouse
  • Recombinant Fusion Proteins
  • NF-KappaB Inhibitor alpha