Yi-Chen Wang1, Chong-Chao Hsieh2, Hsuan-Fu Kuo3, Ming-Kai Tsai4, San-Nan Yang5, Chang-Hung Kuo6, Min-Sheng Lee7, Chih-Hsing Hung8. 1. Division of Cardiology, Department of Internal Medicine, Kaohsiung Armed Forces General Hospital; 2. Division of Cardiac Surgery, Department of Surgery; 3. Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University; 4. Division of Nephrology, Department of Internal Medicine, Kaohsiung Armed Forces General Hospital, Kaohsiung; ; Department of Nursing, MeiHo University, Pingtung; 5. Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University; ; Department of Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung Medical University; ; Department of Pediatrics, Faculty of Pediatrics, College of Medicine, Kaohsiung Medical University; 6. Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University; ; Department of Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung Medical University; ; Department of Pediatrics, Kaohsiung Municipal Ta-Tung Hospital; 7. Department of Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung Medical University; ; Department of Pediatrics, Kaohsiung Municipal Ta-Tung Hospital; 8. Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University; ; Department of Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung Medical University; ; Department of Pediatrics, Faculty of Pediatrics, College of Medicine, Kaohsiung Medical University; ; Department of Pediatrics, Kaohsiung Municipal Hsiao-Kang Hospital, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
Abstract
BACKGROUND: Chemokine is important in the initiation and progression of atherosclerosis, the clinically manifest stages of atherosclerosis and acute coronary syndrome. Vitamin D deficiency has been reportedly linked with hypertension and myocardial infarction, as well as other cardiovascular-related diseases, such as congestive heart failure, peripheral vascular disease and atherosclerosis. Monocyte chemoattractant protein 1 (MCP-1) mediates atherosclerosis and other cardiovascular diseases. However, there have been few studies conducted about the role of 1α,25-(OH)2D3 on MCP-1 expression in human monocytes. METHODS: We investigated the effects of vitamin A, C and 1α,25-(OH)2D3, three common vitamins, to better ascertain MCP-1 expression in human monocyte and also the associated intracellular mechanism. Human monocyte cell line (THP-1 cell) and THP-1 cell-induced macrophage were treated with varying doses of vitamin A, C and 1α,25-(OH)2D3 for 2 hours before LPS stimulation. Supernatants were harvested to measure MCP-1 levels by the enzyme-linked immunosorbent assay (ELISA). The intracellular mechanism about the effects of vitamin A, C and 1α,25-(OH)2D3 on the expression of MCP-1 expression in human monocytes was assessed by western blot. RESULTS: We found that Lipopolysaccharides (LPS)-induced MCP-1 production was suppressed by 1α,25-(OH)2D3 in THP-1 cells and THP-1-induced macrophage. Only high concentration of vitamin A and C could reduce LPS-induced MCP-1 production in THP-1-induced macrophage, but not in THP-1 cells. LPS-induced p38 expression in THP-1 cells was suppressed by 1α,25-(OH)2D3. A selective p38 pathway inhibitor SB203580 could also suppress LPS-induced MCP-1 production. However, vitamin D receptor blocking antibody could reverse the suppressive effect of 1α,25-(OH)2D3 on MCP-1 expression. CONCLUSIONS: These data demonstrate that 1α,25-(OH)2D3 is effective in down-regulating LPS-induced MCP-1. The suppressive effect on MCP-1 may, at least in part, involve the vitamin D receptor and down-regulation of LPS - induced p38 expression. KEY WORDS: Chemokine; Monocyte chemoattractant protein 1 (MCP-1); Monocyte; p38; Vitamin D.
BACKGROUND: Chemokine is important in the initiation and progression of atherosclerosis, the clinically manifest stages of atherosclerosis and acute coronary syndrome. Vitamin D deficiency has been reportedly linked with hypertension and myocardial infarction, as well as other cardiovascular-related diseases, such as congestive heart failure, peripheral vascular disease and atherosclerosis. Monocyte chemoattractant protein 1 (MCP-1) mediates atherosclerosis and other cardiovascular diseases. However, there have been few studies conducted about the role of 1α,25-(OH)2D3 on MCP-1 expression in human monocytes. METHODS: We investigated the effects of vitamin A, C and 1α,25-(OH)2D3, three common vitamins, to better ascertain MCP-1 expression in human monocyte and also the associated intracellular mechanism. Human monocyte cell line (THP-1 cell) and THP-1 cell-induced macrophage were treated with varying doses of vitamin A, C and 1α,25-(OH)2D3 for 2 hours before LPS stimulation. Supernatants were harvested to measure MCP-1 levels by the enzyme-linked immunosorbent assay (ELISA). The intracellular mechanism about the effects of vitamin A, C and 1α,25-(OH)2D3 on the expression of MCP-1 expression in human monocytes was assessed by western blot. RESULTS: We found that Lipopolysaccharides (LPS)-induced MCP-1 production was suppressed by 1α,25-(OH)2D3 in THP-1 cells and THP-1-induced macrophage. Only high concentration of vitamin A and C could reduce LPS-induced MCP-1 production in THP-1-induced macrophage, but not in THP-1 cells. LPS-induced p38 expression in THP-1 cells was suppressed by 1α,25-(OH)2D3. A selective p38 pathway inhibitor SB203580 could also suppress LPS-induced MCP-1 production. However, vitamin D receptor blocking antibody could reverse the suppressive effect of 1α,25-(OH)2D3 on MCP-1 expression. CONCLUSIONS: These data demonstrate that 1α,25-(OH)2D3 is effective in down-regulating LPS-induced MCP-1. The suppressive effect on MCP-1 may, at least in part, involve the vitamin D receptor and down-regulation of LPS - induced p38 expression. KEY WORDS: Chemokine; Monocyte chemoattractant protein 1 (MCP-1); Monocyte; p38; Vitamin D.
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