General Information:

Id: 6,145 (click here to show other Interactions for entry)
Diseases: Diabetes mellitus, type II - [OMIM]
Insulin resistance
Rattus norvegicus
article
Reference: Patterson AJ et al.(2012) Hypoxia-derived oxidative stress mediates epigenetic repression of PKCepsilon gene in foetal rat hearts Cardiovasc. Res. 93: 302-310 [PMID: 22139554]

Interaction Information:

Comment Hypoxia induced in vivo to pregnant rats, ex vivo to isolated foetal rat hearts, and in vitro in the rat embryonic ventricular myocyte cell line H9c2 resulted in a comparable decrease in PKCepsilon protein and mRNA abundance in foetal hearts and H9c2 cells, which was associated with a significant increase in CpG methylation of the SP1-binding sites at the PKCepsilon promoter.
Formal Description
Interaction-ID: 57483

decreases_expression of

gene/protein

PRKCE

via epigenetic repression
Comment In H9c2 cells and foetal hearts, hypoxia caused nuclear accumulation of HIF-1alpha, which was inhibited by 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole and 2-methoxy estradiol. The HIF-1alpha inhibitors had no significant effect on hypoxia-induced PKCepsilon mRNA repression.
Formal Description
Interaction-ID: 57526

increases_quantity of

gene/protein

HIF1A

in nucleus
Drugbank entries Show/Hide entries for HIF1A
Comment Hypoxia produced a time-dependent increase in ROS production in H9c2 cells and foetal hearts that was blocked by ROS scavengers N-acetyl-cysteine or tempol. In accordance, N-acetyl-cysteine and tempol, but not apocynin, inhibited the hypoxic effect and restored PKCepsilon protein and mRNA expression to the control values in foetal hearts and H9c2 cells.
Formal Description
Interaction-ID: 57527

increases_quantity of

drug/chemical compound

Reactive oxygen species

Comment Hypoxia induced in vivo to pregnant rats, ex vivo to isolated foetal rat hearts, and in vitro in the rat embryonic ventricular myocyte cell line H9c2 resulted in a comparable decrease in PKCepsilon protein and mRNA abundance in foetal hearts and H9c2 cells, which was associated with a significant increase in CpG methylation of the SP1-binding sites at the PKCepsilon promoter.
Formal Description
Interaction-ID: 57530