Peptidoglycan recognition protein-S (PGRP-S) is upregulated by NF-kappaB

Neurosci Lett. 2008 Jan 10;430(2):138-41. doi: 10.1016/j.neulet.2007.10.027. Epub 2007 Nov 1.

Abstract

Cerebral ischemia triggers inflammation and apoptosis, and the transcription factor NF-kappaB is a key regulator of both events. Here, we report on the induction of the peptidoglycan recognition protein-S (PGRP-S) in a mouse model of cerebral ischemia. Upregulation was reduced if the NF-kappaB subunit RelA was conditionally deleted in the brain. Regulation of PGRP-S transcription by RelA was confirmed in vitro. Cotransfection of a RelA expression plasmid stimulated the expression of a PGRP-S luciferase fusion gene. Mutation of two NF-kappaB response elements in the PGRP-S promoter disrupted stimulation by RelA. To investigate the function of PGRP-S in cerebral ischemia, we subjected PGRP-S(-/-) mice to cerebral ischemia. However, there was no difference in the infarct size in PGRP-S-deficient mice compared to controls. In summary, the data show that PGRP-S is induced in cerebral ischemia by RelA, but its role in ischemia is unclear.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Brain Ischemia / genetics
  • Brain Ischemia / metabolism
  • Brain Ischemia / pathology
  • Brain Ischemia / physiopathology
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism*
  • Cerebral Cortex / metabolism
  • Cerebral Cortex / pathology
  • Disease Models, Animal
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Knockout
  • Mutation
  • PC12 Cells
  • Rats
  • Transcription Factor RelA / physiology*
  • Transfection
  • Up-Regulation / drug effects
  • Up-Regulation / physiology*

Substances

  • Carrier Proteins
  • Rela protein, mouse
  • Transcription Factor RelA
  • peptidoglycan recognition protein