Expression of microsomal epoxide hydrolase is elevated in Alzheimer's hippocampus and induced by exogenous β-amyloid and trimethyl-tin

Mei Liu, Anyang Sun, Eun Joo Shin, Xianxi Liu, Sang Geon Kim, Cecil R. Runyons, William Markesbery, Hyoung Chun Kim, Guoying Bing

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

Abstract

The brain is a potential target for drugs and environmental toxins. Microsomal epoxide hydrolase (mEH) is one of several critical biotransformation enzymes in xenobiotic metabolism and detoxification. In the present study, we report that the expression of mEH is significantly elevated in the hippocampus and associated cortex, but not in the cerebellum, in Alzheimer's disease (AD) patients. A large proportionq1 of the mEH-positive cells are located around β-amyloid plaques. The mEH-positive-staining cells are astrocytes and pyramidal neurons. Western blotting analysis confirmed increased expression of mEH in AD hippocampal tissues. In primary hippocampal glial culture, β-amyloid aggregation stimulated mEH expression in the astrocytes, which displayed a patchy distribution. An environmental neurotoxic agent, trimethyl-tin, also activated mEH expression in rat hippocampus and entorhinal cortex. The present study demonstrates a significant increase in mEH expression in the AD hippocampus, a region showing abundant neuropathology in AD. The expression of mEH could also be elevated by exposure to exogenous β-amyloid in vitro and environmental toxins in vivo. Our studies suggest that mEH may play a role in pathogenesis of neurodegeneration in response to environmental stress.

Original languageEnglish
Pages (from-to)2027-2034
Number of pages8
JournalEuropean Journal of Neuroscience
Volume23
Issue number8
DOIs
StatePublished - Apr 2006

Keywords

  • Astrocyte
  • Epoxide hydrolase
  • Hippocampus
  • Neurodegeneration

ASJC Scopus subject areas

  • General Neuroscience

Fingerprint

Dive into the research topics of 'Expression of microsomal epoxide hydrolase is elevated in Alzheimer's hippocampus and induced by exogenous β-amyloid and trimethyl-tin'. Together they form a unique fingerprint.

Cite this