Epigallocatechin activates haem oxygenase-1 expression via protein kinase Cδ and Nrf2

Ogborne, Richard M., Rushworth, Stuart and O'Connell, Maria ORCID: https://orcid.org/0000-0002-0267-0951 (2008) Epigallocatechin activates haem oxygenase-1 expression via protein kinase Cδ and Nrf2. Biochemical and Biophysical Research Communications, 373 (4). pp. 584-588. ISSN 1090-2104

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Abstract

The Nrf2/anti-oxidant response element (ARE) pathway plays an important role in regulating cellular anti-oxidants, including haem oxygenase-1 (HO-1). Various kinases have been implicated in the pathways leading to Nrf2 activation. Here, we investigated the effect of epigallocatechin (EGC) on ARE-mediated gene expression in human monocytic cells. EGC time and dose dependently increased HO-1 mRNA and protein expression but had minimal effect on expression of other ARE-regulated genes, including NAD(P)H:quinone oxidoreductase 1, glutathione cysteine ligase and ferritin. siRNA knock down of Nrf2 significantly inhibited EGC-induced HO-1 expression. Furthermore, inhibition of PKC by Ro-31-8220 dose dependently decreased EGC-induced HO-1 mRNA expression, whereas MAP kinase and phosphatidylinositol-3-kinase pathway inhibitors had no significant effect. EGC stimulated phosphorylation of PKCaß and d in THP-1 cells. PKCd inhibition significantly decreased EGC-induced HO-1 mRNA expression, whereas PKCa- and ß-specific inhibitors had no significant effect. These results demonstrate for the first time that EGC-induced HO-1 expression occurs via PKCd and Nrf2.

Item Type: Article
Faculty \ School: Faculty of Science > School of Pharmacy
UEA Research Groups: Faculty of Science > Research Groups > Pharmaceutical Cell Biology (former - to 2017)
Faculty of Medicine and Health Sciences > Research Groups > Cancer Studies
Faculty of Science > Research Groups > Molecular and Tissue Pharmacology
Faculty of Medicine and Health Sciences > Research Centres > Metabolic Health
Depositing User: Rachel Smith
Date Deposited: 17 Mar 2011 11:50
Last Modified: 26 Oct 2023 01:12
URI: https://ueaeprints.uea.ac.uk/id/eprint/26502
DOI: 10.1016/j.bbrc.2008.06.068

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