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Updated: Mar 22, 2026
Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
Published on: August 12, 2019
Effect of Vitamin D3 on Monocyte Chemoattractant Protein 1 Production in Monocytes and Macrophages
Yi-Chen Wang1, Chong-Chao Hsieh2, Hsuan-Fu Kuo3
1Division of Cardiology, Department of Internal Medicine, Kaohsiung Armed Forces General Hospital;
Insights
Vitamin D (1α,25-(OH)2D3) effectively reduces Monocyte Chemoattractant Protein 1 (MCP-1) production in human monocytes. This effect involves the vitamin D receptor and the p38 signaling pathway, offering insights into atherosclerosis management.
Area of Science:
- Immunology
- Endocrinology
- Cardiovascular Research
Background:
- Chemokines, particularly Monocyte Chemoattractant Protein 1 (MCP-1), play a critical role in atherosclerosis development and progression.
- Vitamin D deficiency is associated with cardiovascular diseases, including hypertension, myocardial infarction, and atherosclerosis.
- The specific role of 1α,25-(OH)2D3 in regulating MCP-1 expression in human monocytes remains under-investigated.
Purpose of the Study:
- To investigate the effects of 1α,25-(OH)2D3, vitamin A, and vitamin C on MCP-1 expression in human monocytes.
- To elucidate the intracellular mechanisms underlying the regulation of MCP-1 by these vitamins.
Main Methods:
- Human monocyte cell line (THP-1) and induced macrophages were treated with varying doses of vitamins A, C, and 1α,25-(OH)2D3.
- MCP-1 levels were quantified using ELISA post-LPS stimulation.
- Intracellular mechanisms were assessed via western blot, including p38 expression and vitamin D receptor involvement.
Main Results:
- 1α,25-(OH)2D3 significantly suppressed Lipopolysaccharides (LPS)-induced MCP-1 production in both THP-1 cells and macrophages.
- High concentrations of vitamins A and C showed limited suppression of MCP-1 in macrophages only.
- 1α,25-(OH)2D3 suppressed LPS-induced p38 expression, an effect reversible by vitamin D receptor blockade.
Conclusions:
- 1α,25-(OH)2D3 demonstrates efficacy in down-regulating LPS-induced MCP-1 expression in human monocytes.
- The observed suppressive effect of 1α,25-(OH)2D3 on MCP-1 is mediated, at least partly, through the vitamin D receptor and the down-regulation of p38 expression.
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.
