Effects of apoE genotype on macrophage inflammation and heme oxygenase-1 expression

Jofre-Monseny, Laia, Loboda, Agnieszka, Wagner, Anika E., Huebbe, Patricia, Boesch-Saadatmandi, Christine, Jozkowicz, Alicja, Minihane, Anne Marie ORCID: https://orcid.org/0000-0001-9042-4226, Dulak, Jozef and Rimbach, Gerald (2007) Effects of apoE genotype on macrophage inflammation and heme oxygenase-1 expression. Biochemical and Biophysical Research Communications, 357 (1). pp. 319-324. ISSN 1090-2104

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Abstract

In order to gain a more comprehensive understanding of the aetiology of apolipoprotein E4 genotype-cardiovascular disease (CVD) associations, the impact of the apoE genotype on the macrophage inflammatory response was examined. The murine monocyte–macrophage cell line (RAW 264.7) stably transfected to produce equal amounts of human apoE3 or apoE4 was used. Following LPS stimulation, apoE4-macrophages showed higher and lower concentrations of tumour necrosis factor alpha (pro-inflammatory) and interleukin 10 (anti-inflammatory), respectively, both at mRNA and protein levels. In addition, increased expression of heme oxygenase-1 (a stress-induced anti-inflammatory protein) was observed in the apoE4-cells. Furthermore, in apoE4-macrophages, an enhanced transactivation of the key redox sensitive transcription factor NF-κB was shown. Current data indicate that apoE4 macrophages have an altered inflammatory response, which may contribute to the higher CVD risk observed in apoE4 carriers.

Item Type: Article
Faculty \ School: Faculty of Medicine and Health Sciences > Norwich Medical School
UEA Research Groups: Faculty of Medicine and Health Sciences > Research Groups > Nutrition and Preventive Medicine
Faculty of Medicine and Health Sciences > Research Groups > Cardiovascular and Metabolic Health
Faculty of Medicine and Health Sciences > Research Centres > Lifespan Health
Depositing User: Rhiannon Harvey
Date Deposited: 31 May 2011 15:46
Last Modified: 19 Oct 2023 00:46
URI: https://ueaeprints.uea.ac.uk/id/eprint/31639
DOI: 10.1016/j.bbrc.2007.03.150

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