Cerebral protein kinase C and its mRNA level in apolipoprotein E-deficient mice

Mei Chu Hung, Kaoru Hayase, Riki Yoshida, Masao Sato, Katsumi Imaizumi

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

It is known that protein kinase C (PKC) activity may be one of the fundamental cellular changes associated with memory function. Apolipoprotein E (apoE) deficiency causes cholinergic deficits and memory impairment. ApoE-deficient mouse has been employed as a serviceable model for studying the relation between apoE and the memory deficit induced by cholinergic impairment. Brain-fatty acid binding protein (b-FABP) might be functional during development of the nervous system. Peroxisome proliferator-activated receptor (PPAR) is involved in the early change in lipid metabolism. We investigated the alterations not only in cerebral PKC activity, but also in the gene expressions of PKC-β, brain-FABP and PPAR-α in apoE-deficient mice. The results showed that there was a lower cerebral membrane-bound PKC activity in the apoE-deficient mice than in its wild type strain (C57BL/6). But there were no significant differences in cytosolic PKC activity. PKC-β, b-FABP and PPAR-α mRNA expressions in cerebrum were lowered in apoE-deficient mice. These findings may be involved in the dysfunction of the brain neurotransmission system in apoE-deficient mouse. Alternatively, these results also suggest that cerebral apoE plays an important role in brain PKC activation by maintaining an appropriate expression of b-FABP and PPAR-α mRNAs.

Original languageEnglish
Pages (from-to)1419-1427
Number of pages9
JournalLife Sciences
Volume69
Issue number12
DOIs
Publication statusPublished - Aug 10 2001

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

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