Vitamin A supplementation reduces IL-17 and RORc gene expression in atherosclerotic patients.
Vitamin A is a potential mediator of T helper cells in atherosclerosis. The purpose of this study was to evaluate the effect of vitamin A supplementation on expression of Th17 cells-related IL-17 and RORc genes in atherosclerotic patients. Thirty one atherosclerotic patients and 15 healthy controls were studied for 4 months. Atherosclerotic patients were randomly divided into vitamin A or placebo groups. Healthy controls and patients in vitamin A group received 25,000 IU retinyl palmitate per day. Peripheral blood mononuclear cells were isolated, cultured and divided into three groups including fresh cells, phytohemagglutinin (PHA)-activated T cells and ox-LDL-activated T cells. Gene expressions of T cells were studied by real-time PCR. In atherosclerotic patients, vitamin A supplementation resulted in significant decrease in IL-17 gene expression by 0.63-fold in fresh cell, 0.82-fold in PHA-activated cells and 0.65-fold in ox-LDL-activated cells (P < 0.05 for all). RORc gene expression in fresh cells as well as ox-LDL-activated cells decreased significantly after vitamin A supplementation in atherosclerotic patients (P = 0.0001 for both). In PHA-activated cells, vitamin A supplementation significantly decreased RORc gene in both atherosclerotic patients and healthy subjects by 0.87-fold and 0.72, respectively, while in placebo group, the RORc gene expression significantly increased by 1.17-fold (P < 0.05 for all). Findings of this study suggest that vitamin A supplementation may be an effective approach to slow progression of atherosclerosis.
Obesity Research Center, Nutrition and Endocrine Research Center, Research Institute of Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
A
A
Mottaghi
S
S
Ebrahimof
P
P
Angoorani
A-A
AA
Saboor-Yaraghi
D050197:Atherosclerosis / Q000188:drug therapy* / Q000276:immunology; D019587:Dietary Supplements; D005260:Female; D015870:Gene Expression / Q000187:drug effects*; D006801:Humans; D020381:Interleukin-17 / Q000235:genetics*; D008077:Lipoproteins, LDL; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D008875:Middle Aged; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics*; D010835:Phytohemagglutinins; D012333:RNA, Messenger / Q000096:biosynthesis; D058504:Th17 Cells / Q000187:drug effects / Q000276:immunology*; D014801:Vitamin A / Q000008:administration & dosage*
D020381:Interleukin-17; D008077:Lipoproteins, LDL; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D010835:Phytohemagglutinins; D012333:RNA, Messenger; C539900:RORC protein, human; C099252:oxidized low density lipoprotein; D014801:Vitamin A