Endogenous apolipoprotein E suppresses LPS-stimulated microglial nitric oxide production.

Published

Journal Article

The human apolipoprotein (apo) E4 isoform is associated with an increased risk for Alzheimer's disease (AD) and poor prognosis after acute CNS injury. Addition of human apoE inhibits murine microglial activation in culture, suggesting that microglia might be an important physiological target of apoE. In the present study, we examined the role of endogenous murine apoE in modulating microglial nitric oxide (NO) production following lipopolysaccharide (LPS) stimulation. Brain cultures from apoE-deficient mouse pups showed enhanced NO production relative to cultures from wild-type mice and from transgenic mice expressing the human apoE3 isoform, demonstrating that endogenous apoE produced by glial cultures is capable of inhibiting microglial function. ApoE produced within the brain may suppress microglial reactivity and thus alter the CNS response to acute and chronic injury.

Full Text

Duke Authors

Cited Authors

  • Laskowitz, DT; Matthew, WD; Bennett, ER; Schmechel, D; Herbstreith, MH; Goel, S; McMillian, MK

Published Date

  • March 9, 1998

Published In

Volume / Issue

  • 9 / 4

Start / End Page

  • 615 - 618

PubMed ID

  • 9559926

Pubmed Central ID

  • 9559926

International Standard Serial Number (ISSN)

  • 0959-4965

Language

  • eng

Conference Location

  • England