title: Catechin reduces atherosclerotic lesion development in apo E-deficient mice: a transcriptomic study.
abstract: Much experimental evidence supports a protective role of dietary flavonoids against cardiovascular diseases. The aim of the present study was to investigate the anti-atherosclerotic effects of catechin supplemented in the diet of apoE deficient mice at a low nutritional level and to explore the mechanisms of action by a transcriptomic approach. After 6 weeks of supplementation, atherosclerotic lesions were assessed by histomorphometry and several markers of lipid, inflammation and oxidative stress status were evaluated. Analysis of the global gene expression in the aorta was carried out using pangenomic arrays. Catechin supplementation reduced the mean atherosclerotic lesion area by 32% but had no effect on total cholesterol and triacylglycerol levels in the plasma and the liver. The plasma antioxidant capacity (FRAP) and inflammatory status (serum amyloid A) were unchanged. The expression of 450 genes was significantly modified by catechin supplementation. Some of the most significantly down-regulated genes included genes coding for adhesion molecules such as CD34 and PSGL-1 known to play a key role in leukocyte adhesion to the endothelium. Other genes involved in energy metabolism, lipid metabolism and lipids trafficking such as FABP4, LPL and SCARA5 were down-regulated and may contribute to the atheroprotective effect of catechin. This work shows that transcriptomic allows characterizing the biological effects of low doses of flavonoids where common markers were not significantly affected.
authors.affiliation: Unité de Nutrition Humaine UMR1019, INRA-Clermont Ferrand/Theix, 63122 Saint Genès Champanelle, France.
authors.forename: Sylvain
authors.initials: S
authors.lastname: Auclair
authors.forename: Dragan
authors.initials: D
authors.lastname: Milenkovic
authors.forename: Catherine
authors.initials: C
authors.lastname: Besson
authors.forename: Stéphanie
authors.initials: S
authors.lastname: Chauvet
authors.forename: Elyett
authors.initials: E
authors.lastname: Gueux
authors.forename: Christine
authors.initials: C
authors.lastname: Morand
authors.forename: Andrzej
authors.initials: A
authors.lastname: Mazur
authors.forename: Augustin
authors.initials: A
authors.lastname: Scalbert
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001018:Aortic Diseases / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics; D050197:Atherosclerosis / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D002392:Catechin / Q000494:pharmacology*; D019587:Dietary Supplements; D004195:Disease Models, Animal; D018450:Disease Progression; D020869:Gene Expression Profiling / Q000379:methods; D005786:Gene Expression Regulation / Q000187:drug effects; D007249:Inflammation / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control; D018836:Inflammation Mediators / Q000097:blood; D008055:Lipids / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D020411:Oligonucleotide Array Sequence Analysis; D016133:Polymerase Chain Reaction; D000685:Serum Amyloid A Protein / Q000378:metabolism
chemical_list: D000975:Antioxidants; D001057:Apolipoproteins E; D018836:Inflammation Mediators; D008055:Lipids; D000685:Serum Amyloid A Protein; D002392:Catechin