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Effects of dietary carotenoids on mouse lung genomic profiles and their modulatory effects on short-term cigarette smoke exposures.

Aung HH, Vasu VT, Valacchi G, Corbacho AM, Kota RS, Lim Y, Obermueller-Jevic UC, Packer L, Cross CE, Gohil K - Genes Nutr (2008)

Bottom Line: Four weeks of dietary supplementations results in plasma and lung carotenoid (CAR) concentrations that approximated the levels detected in humans.Bioactivity of the CARs was determined by assaying their effects on the activity of the lung transcriptome (~8,500 mRNAs).These genes encoded inflammatory-immune proteins.

View Article: PubMed Central - PubMed

Affiliation: Center for Comparative Respiratory Biology and Medicine, Clinical Nutrition and Vascular Medicine, Genome and Biomedical Sciences Facility, University of California, 6404A, 451 East Health Sciences Drive, Davis, CA, 95616, USA.

ABSTRACT
Male C57BL/6 mice were fed diets supplemented with either beta-carotene (BC) or lycopene (LY) that were formulated for human consumption. Four weeks of dietary supplementations results in plasma and lung carotenoid (CAR) concentrations that approximated the levels detected in humans. Bioactivity of the CARs was determined by assaying their effects on the activity of the lung transcriptome (~8,500 mRNAs). Both CARs activated the cytochrome P450 1A1 gene but only BC induced the retinol dehydrogenase gene. The contrasting effects of the two CARs on the lung transcriptome were further uncovered in mice exposed to cigarette smoke (CS) for 3 days; only LY activated ~50 genes detected in the lungs of CS-exposed mice. These genes encoded inflammatory-immune proteins. Our data suggest that mice offer a viable in vivo model for studying bioactivities of dietary CARs and their modulatory effects on lung genomic expression in both health and after exposure to CS toxicants.

No MeSH data available.


Related in: MedlinePlus

“Heat-map” inflammation-immune related genes in the lungs of mice fed the 3 assigned diets. Each column represents a mouse and each row a gene. Three distinct patterns of expression could be identified. Cluster I shows high expression only in the CS-exposed lungs of LY fed mice. Cluster II shows medium-expression of genes in air breathing, BC fed mice and the expression was suppressed by CS. The expression of the same cluster of genes was low in air breathing mice fed LY but was induced when the mice were exposed to CS. Cluster III shows similar expression in mice fed the basal or the BC-supplemented diet but the expression is reversed in the mice fed the LY-supplemented diet
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Fig6: “Heat-map” inflammation-immune related genes in the lungs of mice fed the 3 assigned diets. Each column represents a mouse and each row a gene. Three distinct patterns of expression could be identified. Cluster I shows high expression only in the CS-exposed lungs of LY fed mice. Cluster II shows medium-expression of genes in air breathing, BC fed mice and the expression was suppressed by CS. The expression of the same cluster of genes was low in air breathing mice fed LY but was induced when the mice were exposed to CS. Cluster III shows similar expression in mice fed the basal or the BC-supplemented diet but the expression is reversed in the mice fed the LY-supplemented diet

Mentions: The major novel discovery of this in vivo genome-wide screen is the identification of a large cluster of inflammatory-immune genes that are induced by dietary LY but not BC in the lungs of CS-exposed mice (Fig. 6). Three distinct clusters of genes could be identified in this group of inflammatory-immune genes. Cluster I (2 genes) showed low expression in the lungs of all mice except those that were fed LY-supplemented diet and exposed to CS; these two genes are frequently used as markers of neutrophils [8, 70]. A large sub-group of 24 genes, cluster II, Fig. 6, was moderately expressed in the lungs of mice fed the basal diet or the BC-supplemented diet. The lungs of BC-supplemented mice breathing air showed higher expression of this cluster of genes when compared to that in the lungs of other groups of mice breathing air. Their expressions were suppressed by exposure to CS. In contrast to the suppressing effects of CS on these cluster II genes in mice fed the basal or the BC diet, the LY fed mice showed obvious augmentation of their expression. Inductions of Cal A, Cal B, Slfn4, IL1β, and carbonyl reductase 3 (Cbr3) genes in CS breathing lungs of mice fed LY-supplemented diet and suppression of these genes in the CS breathing lungs of mice fed BC-supplemented diet were independently confirmed by qRT- PCR (Fig. 7a–c). Genes in cluster III behave like those in cluster II except that they were highly expressed in the lungs of air breathing mice fed the basal or the BC diets.Fig. 6


Effects of dietary carotenoids on mouse lung genomic profiles and their modulatory effects on short-term cigarette smoke exposures.

Aung HH, Vasu VT, Valacchi G, Corbacho AM, Kota RS, Lim Y, Obermueller-Jevic UC, Packer L, Cross CE, Gohil K - Genes Nutr (2008)

“Heat-map” inflammation-immune related genes in the lungs of mice fed the 3 assigned diets. Each column represents a mouse and each row a gene. Three distinct patterns of expression could be identified. Cluster I shows high expression only in the CS-exposed lungs of LY fed mice. Cluster II shows medium-expression of genes in air breathing, BC fed mice and the expression was suppressed by CS. The expression of the same cluster of genes was low in air breathing mice fed LY but was induced when the mice were exposed to CS. Cluster III shows similar expression in mice fed the basal or the BC-supplemented diet but the expression is reversed in the mice fed the LY-supplemented diet
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2654053&req=5

Fig6: “Heat-map” inflammation-immune related genes in the lungs of mice fed the 3 assigned diets. Each column represents a mouse and each row a gene. Three distinct patterns of expression could be identified. Cluster I shows high expression only in the CS-exposed lungs of LY fed mice. Cluster II shows medium-expression of genes in air breathing, BC fed mice and the expression was suppressed by CS. The expression of the same cluster of genes was low in air breathing mice fed LY but was induced when the mice were exposed to CS. Cluster III shows similar expression in mice fed the basal or the BC-supplemented diet but the expression is reversed in the mice fed the LY-supplemented diet
Mentions: The major novel discovery of this in vivo genome-wide screen is the identification of a large cluster of inflammatory-immune genes that are induced by dietary LY but not BC in the lungs of CS-exposed mice (Fig. 6). Three distinct clusters of genes could be identified in this group of inflammatory-immune genes. Cluster I (2 genes) showed low expression in the lungs of all mice except those that were fed LY-supplemented diet and exposed to CS; these two genes are frequently used as markers of neutrophils [8, 70]. A large sub-group of 24 genes, cluster II, Fig. 6, was moderately expressed in the lungs of mice fed the basal diet or the BC-supplemented diet. The lungs of BC-supplemented mice breathing air showed higher expression of this cluster of genes when compared to that in the lungs of other groups of mice breathing air. Their expressions were suppressed by exposure to CS. In contrast to the suppressing effects of CS on these cluster II genes in mice fed the basal or the BC diet, the LY fed mice showed obvious augmentation of their expression. Inductions of Cal A, Cal B, Slfn4, IL1β, and carbonyl reductase 3 (Cbr3) genes in CS breathing lungs of mice fed LY-supplemented diet and suppression of these genes in the CS breathing lungs of mice fed BC-supplemented diet were independently confirmed by qRT- PCR (Fig. 7a–c). Genes in cluster III behave like those in cluster II except that they were highly expressed in the lungs of air breathing mice fed the basal or the BC diets.Fig. 6

Bottom Line: Four weeks of dietary supplementations results in plasma and lung carotenoid (CAR) concentrations that approximated the levels detected in humans.Bioactivity of the CARs was determined by assaying their effects on the activity of the lung transcriptome (~8,500 mRNAs).These genes encoded inflammatory-immune proteins.

View Article: PubMed Central - PubMed

Affiliation: Center for Comparative Respiratory Biology and Medicine, Clinical Nutrition and Vascular Medicine, Genome and Biomedical Sciences Facility, University of California, 6404A, 451 East Health Sciences Drive, Davis, CA, 95616, USA.

ABSTRACT
Male C57BL/6 mice were fed diets supplemented with either beta-carotene (BC) or lycopene (LY) that were formulated for human consumption. Four weeks of dietary supplementations results in plasma and lung carotenoid (CAR) concentrations that approximated the levels detected in humans. Bioactivity of the CARs was determined by assaying their effects on the activity of the lung transcriptome (~8,500 mRNAs). Both CARs activated the cytochrome P450 1A1 gene but only BC induced the retinol dehydrogenase gene. The contrasting effects of the two CARs on the lung transcriptome were further uncovered in mice exposed to cigarette smoke (CS) for 3 days; only LY activated ~50 genes detected in the lungs of CS-exposed mice. These genes encoded inflammatory-immune proteins. Our data suggest that mice offer a viable in vivo model for studying bioactivities of dietary CARs and their modulatory effects on lung genomic expression in both health and after exposure to CS toxicants.

No MeSH data available.


Related in: MedlinePlus