Vitamin E inhibits CD36 scavenger receptor expression in hypercholesterolemic rabbits

Özer, Nesrin Kartal; Negis, Yesim; Aytan, Nurgül; Villacorta, Luis; Ricciarelli, Roberta; Zingg, Jean Marc; Azzi, Angelo

doi:10.1016/j.atherosclerosis.2005.03.050

Cited by 60 publications

(57 citation statements)

References 38 publications

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“…The results of the present association study, together with previous data showing that a-tocopherol is able to modulate CD36 gene expression (40)(41)(42)(43), suggest that the scavenger receptor CD36/FAT, best known for its involvement in long-chain FA uptake by adipose tissue (44)(45)(46)(47), might also be involved in the metabolism of vitamin E. The mechanism by which CD36 affects blood vitamin E concentrations is not known. CD36 recognizes a broad variety of lipid ligands, including FAs, oxidized LDL, apoptotic cells, and b-carotene (48).…”

Section: Discussionmentioning

confidence: 49%

Polymorphisms in the CD36/FAT gene are associated with plasma vitamin E concentrations in humans

Lecompte

Edelenyi

Goumidi

et al. 2011

The American Journal of Clinical Nutrition

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Background: Blood vitamin E concentrations are modulated by dietary, metabolic, and genetic factors. CD36 (cluster of differentiation 36), a class B scavenger receptor, might be involved in tissue vitamin E uptake and thus would influence blood vitamin E concentrations. Objective: The goal of the study was to assess the association between CD36 single nucleotide polymorphisms (SNPs) and plasma a-tocopherol concentrations in humans. Design: A subsample from the adult SU.VI.MAX (SUpplementation en VItamines et Minéraux AntioXydants) cohort (n = 621) and the adolescent cross-sectional HELENA (Healthy Lifestyle in Europe by Nutrition in Adolescence) Study (n = 993) were genotyped for CD36 SNPs (4 and 10 SNPs, respectively). Fasting plasma a-tocopherol concentrations were assayed by using HPLC. Associations were determined by haplotype analyses and by general linear regression models. Results: In the SU.VI.MAX subsample, haplotype analyses showed that some haplotypes of SNPs rs1984112, rs1527479, rs7755, and rs1527483 tended to be associated with plasma a-tocopherol concentrations (P = 0.08 and P = 0.09 for haplotypes 1222 and 1122, respectively). We then investigated the whole known common genetic variability (10 SNPs) of CD36 in the HELENA Study. Three SNPs were associated with lower plasma a-tocopherol concentrations (rs1984112: 23.2%, P = 0.053; rs1761667: 22.9%, P = 0.046; rs1527479: 23.7%, P = 0.0061). After correction for multiple testing, the association between rs1527479 and a-tocopherol concentrations remained significant. This association was modulated by concentrations of fasting serum triglycerides (P for interaction = 0.006) and long-chain polyunsaturated fatty acids (P for interaction = 0.005). Conclusion: Our results suggest that CD36 can modulate blood a-tocopherol concentrations and may therefore be involved in the intestinal absorption or tissue uptake of vitamin E.Am J Clin Nutr 2011;93:644-51.

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Section: Discussionmentioning

confidence: 49%

Polymorphisms in the CD36/FAT gene are associated with plasma vitamin E concentrations in humans

Lecompte

Edelenyi

Goumidi

et al. 2011

The American Journal of Clinical Nutrition

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“…In animals, vitamin E deficiency causes derangement of nucleic acid metabolism (30,31). These results show that serum vitamin E is a determinant of bone mass through its regulation of osteoclast fusion.…”

Section: Vitamin E Has a Gene Regulatory Function That May Delay The mentioning

confidence: 85%

Vitamin E slows down the progression of osteoarthritis

Zhang

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Osteoarthritis is a chronic degenerative joint disorder with the characteristics of articular cartilage destruction, subchondral bone alterations and synovitis. Clinical signs and symptoms of osteoarthritis include pain, stiffness, restricted motion and crepitus. It is the major cause of joint dysfunction in developed nations and has enormous social and economic consequences. Current treatments focus on symptomatic relief, however, they lack efficacy in controlling the progression of this disease, which is a leading cause of disability. Vitamin E is safe to use and may delay the progression of osteoarthritis by acting on several aspects of the disease. In this review, how vitamin E may promote the maintenance of skeletal muscle and the regulation of nucleic acid metabolism to delay osteoarthritis progression is explored. In addition, how vitamin E may maintain the function of sex organs and the stability of mast cells, thus conferring a greater resistance to the underlying disease process is also discussed. Finally, the protective effect of vitamin E on the subchondral vascular system, which decreases the reactive remodeling in osteoarthritis, is reviewed.

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“…Oxidized LDL is found to increase the expression of scavenger receptor CD36. Vitamin-E is found to prevent cholesterol induced atherosclerotic lesions and the induction of CD36 mRNA expression [17]. There are also evidences suggesting that α-tocopherol decrease CD36 expression [11].…”

Section: Resultsmentioning

confidence: 99%

“…α-Tocopherol found to inhibit oxLDL uptake by a mechanism involving downregulation of CD36 mRNA and protein expression. There are other studies as well favoring that Vitamin E inhibits the expression of scavenger receptor CD36 in hypercholesterolemic rabbits [19]. Effect of alpha tocopherol is also studied in human monocyte-derived macrophages which showed that alpha tocopherol enrichment results in decreased CD36 expression and decreased cholesteryl accumulation [11].…”

Section: Resultsmentioning

confidence: 99%

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Studies on Scavenger Receptors under Experimental Hypercholesterolemia: Modulation on Selenium Supplementation

Kaur

Bansal

2010

Biol Trace Elem Res

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Scavenger receptors (SR) are the cell surface proteins that can bind and internalize modified lipoproteins. Because ox-LDL seems to play a key role in foam cell formation during atherogenesis, SR may be critical for pathogenesis of atherosclerosis. The present study was aimed to study the effect of selenium (Se) supplementation on SR, i.e., SRB1 and CD36 under experimental hypercholesterolemia. Male Sprague Dawley rats were divided into three groups and fed on the control diet, high cholesterol diet (HCD), and HCD + Se, respectively, for a period of 4 months. Selenium and reactive oxygen species (ROS) levels were estimated in serum and liver respectively. mRNA expression using RT-PCR and protein expression using ELISA were analyzed for SRB1 and CD36 receptors. Selenium levels decreased whereas ROS levels increased under experimental hypercholesterolemic state. Selenium supplementation (1 ppm), however, diminished the HCD-induced ROS levels. Furthermore, the protein expression of SRB1 was significantly reduced in HCD group in comparison to the control group. On the other hand, HCD-induced increase in CD36 mRNA and protein expression decreased significantly on Se supplementation. In conclusion, CD36 receptors seem to play a pro-atherogenic role under hypercholesterolemic state. Selenium supplementation, in addition, might prove to be a therapeutically valuable approach in near future to limit the adverse effect of hypercholesterolemia.

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Vitamin E inhibits CD36 scavenger receptor expression in hypercholesterolemic rabbits

Cited by 60 publications

References 38 publications

Polymorphisms in the CD36/FAT gene are associated with plasma vitamin E concentrations in humans

Polymorphisms in the CD36/FAT gene are associated with plasma vitamin E concentrations in humans

Vitamin E slows down the progression of osteoarthritis

Studies on Scavenger Receptors under Experimental Hypercholesterolemia: Modulation on Selenium Supplementation

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