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Smoking, Atherosclerosis, and MCP‐1 Expression
Author(s) -
Wong Lina,
Yuan Hongwei,
MartinsGreen Manuela
Publication year - 2004
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1111/j.1067-1927.2004.0abstractcr.x
Subject(s) - chemokine , vasa vasorum , ccr2 , blood vessel , medicine , ccl2 , smoke , carboxyhemoglobin , immunology , inflammation , pathology , chemistry , chemokine receptor , biochemistry , organic chemistry , carbon monoxide , catalysis
The inflammatory events of atherosclerosis involve monocytes, endothelial cells, smooth muscle cells, and several cytokines, including chemokines. Atherosclerosis begins with recruitment of circulating monocytes to sites of blood vessel injury. In the vessel wall, these cells are activated to become macrophages that scavenge toxic material such as oxidized LDL and transition into “foam cells” which will eventually lead to plaque formation. Tobacco smoke is known to exacerbate cardiovascular disease but the mechanisms by which this occurs are not known. The chemokine MCP‐1 is involved in recruiting monocytes to the injured blood vessel wall and is commonly found in atherosclerotic plaques. Our data show that both “first‐hand” and “second‐hand” cigarette smoke stimulate MCP‐1 production in cultured primary human aortic endothelial cells (EC), suggesting that cigarette smoke may contribute to plaque formation by stimulating aortic EC to produce MCP‐1 in blood vessels after smoke injury. To test whether MCP‐1 links smoking and cardiovascular disease, we are studying the expression of this molecule in mice that are either transgenic for human ApoB or are null for MCP‐1 or its receptor, CCR2, by exposing the mice to smoke in a way that closely resembles human smoking. Blood samples from the mice were tested for carboxyhemoglobin, triglycerides, LDL and HDL, and MCP‐1 at successive weeks after initiation of smoking and the aortas isolated to analyze for plaque size and MCP‐1 expression in the tissue. The carboxyhemoglobin test shows that the mice are exposed to smoke. Plasma MCP‐1 and HDL levels are reduced in the smoking groups, whereas LDL, triglyceride, and total cholesterol remain unchanged. On one hand, the decrease in circulating HDL levels suggests that the reason smokers develop atherosclerosis may be because the rate of cholesterol clearance is slowed down. On the other hand, a decrease in circulating MCP‐1 level may reflect that this chemokine accumulates in blood vessel walls, conferring stronger ability for attraction of monocytes. This work is supported by TRDRP and Phillip Morris.