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Research Article Free access | 10.1172/JCI116495

Genetic control of inflammatory gene induction and NF-kappa B-like transcription factor activation in response to an atherogenic diet in mice.

F Liao, A Andalibi, F C deBeer, A M Fogelman, and A J Lusis

Department of Medicine, University of California Los Angeles (UCLA) School of Medicine 90024-1679.

Find articles by Liao, F. in: PubMed | Google Scholar

Department of Medicine, University of California Los Angeles (UCLA) School of Medicine 90024-1679.

Find articles by Andalibi, A. in: PubMed | Google Scholar

Department of Medicine, University of California Los Angeles (UCLA) School of Medicine 90024-1679.

Find articles by deBeer, F. in: PubMed | Google Scholar

Department of Medicine, University of California Los Angeles (UCLA) School of Medicine 90024-1679.

Find articles by Fogelman, A. in: PubMed | Google Scholar

Department of Medicine, University of California Los Angeles (UCLA) School of Medicine 90024-1679.

Find articles by Lusis, A. in: PubMed | Google Scholar

Published June 1, 1993 - More info

Published in Volume 91, Issue 6 on June 1, 1993
J Clin Invest. 1993;91(6):2572–2579. https://doi.org/10.1172/JCI116495.
© 1993 The American Society for Clinical Investigation
Published June 1, 1993 - Version history
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Abstract

A high fat, high cholesterol "atherogenic" diet induced considerably greater hepatic levels of conjugated dienes and expression of several inflammatory and oxidative stress responsive genes (JE, the mouse homologue of monocyte chemotactic protein-1, colony-stimulating factors, heme oxygenase, and members of the serum amyloid A family) in fatty streak susceptible C57BL/6 mice compared to fatty streak resistant C3H/HeJ mice. Since serum amyloid A proteins bind exclusively to HDL and influence the properties of HDL, serum amyloid A expression may contribute to the decrease in HDL levels seen in the susceptible strains. Induction of a similar set of genes was observed upon injection of minimally oxidized low density lipoprotein. The transcription factor NF-kappa B is known to be activated by oxidative stress and is involved in the transcriptional regulation of several of these genes. On the atherogenic diet the susceptible C57BL/6 mice exhibited significant NF-kappa B-like activation whereas the resistant C3H/HeJ mice exhibited little or no activation. These results are consistent with the hypothesis that the atherogenic diet resulted in the accumulation of oxidized lipids in certain tissues (e.g., liver and arteries) and the resulting inflammatory response to this oxidative stress was genetically determined.

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