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Aspirin prevents adhesion of T lymphoblasts to vascular smooth muscle cells
Author(s) -
Yotsui Takamori,
Yasuda Osamu,
Kawamoto Hidenobu,
Higuchi Masayoshi,
Chihara Yukana,
Umemoto Eiji,
Tanaka Toshiyuki,
Miyasaka Masayuki,
Rakugi Hiromi,
Ogihara Toshio
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.12.052
Subject(s) - lymphoblast , vascular smooth muscle , aspirin , adhesion , chemistry , microbiology and biotechnology , smooth muscle , medicine , biochemistry , biology , cell culture , genetics , organic chemistry
In the development of atherosclerosis, inflammatory cells adhere to and migrate into the vascular walls by interacting with vascular smooth muscle cells. To investigate the mechanism of aspirin's anti‐atherogenic activity, we examined whether aspirin inhibits the adhesion of lymphocytes to human aortic smooth muscle cells (AoSMC). Aspirin inhibited T‐cell adhesion to AoSMC activated by interleukin 1β (IL‐1β) in a dose‐dependent manner. Antibodies to the adhesion molecules ICAM‐1 or VCAM‐1, but not to E‐selectin, prevented T‐cell adhesion. ICAM‐1 and VCAM‐1 expression stimulated by IL‐1β was reduced by the treatment with aspirin, whereas the expression of E‐selectin was unaffected. Nuclear factor κB (NF‐κB) activity was enhanced by IL‐1β and reduced by aspirin, indicating that decreased ICAM‐1 and VCAM‐1 expression was due to reduced NF‐κB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL‐1β‐activated AoSMC by reducing NF‐κB activity and decreasing expression of ICAM‐1 and VCAM‐1, and may prevent the development of atherosclerosis.