Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 400708
Title Knockout of the Bcmo1 gene results in an inflammatory response in female lung, which is suppressed by dietary beta-carotene
Author(s) Helden, Y.G.J.; Heil, S.G.; Schooten, F.J. van; Kramer, E.; Hessel, S.; Amengual, J.; Ribot, J.; Teerds, K.J.; Wyss, A.; Lietz, G.; Bonet, M.L.; Lintig, J. von; Godschalk, R.W.L.; Keijer, J.
Source Cellular and Molecular Life Sciences 67 (2010)12. - ISSN 1420-682X - p. 2039 - 2056.
Department(s) RIKILT - Business Unit Safety & Health
Human and Animal Physiology
Publication type Refereed Article in a scientific journal
Publication year 2010
Keyword(s) nonsteroidal antiinflammatory drugs - retinol efficacy trial - vitamin-a-deficiency - cardiovascular-disease - alcohol-dehydrogenase - double-tracer - acid - cancer - cells - mice
Abstract Beta-carotene 15,15'-monooxygenase 1 knockout (Bcmo1 (-/-)) mice accumulate beta-carotene (BC) similarly to humans, whereas wild-type (Bcmo1 (+/+)) mice efficiently cleave BC. Bcmo1 (-/-) mice are therefore suitable to investigate BC-induced alterations in gene expression in lung, assessed by microarray analysis. Bcmo1 (-/-) mice receiving control diet had increased expression of inflammatory genes as compared to BC-supplemented Bcmo1 (-/-) mice and Bcmo1 (+/+) mice that received either control or BC-supplemented diets. Differential gene expression in Bcmo1 (-/-) mice was confirmed by real-time quantitative PCR. Histochemical analysis indeed showed an increase in inflammatory cells in lungs of control Bcmo1 (-/-) mice. Supported by metabolite and gene-expression data, we hypothesize that the increased inflammatory response is due to an altered BC metabolism, resulting in an increased vitamin A requirement in Bcmo1 (-/-) mice. This suggests that effects of BC may depend on inter-individual variations in BC-metabolizing enzymes, such as the frequently occurring human polymorphisms in BCMO1.
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