Aspirin prevents adhesion of T lymphoblasts to vascular smooth muscle cells |
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Authors: | Yotsui Takamori Yasuda Osamu Kawamoto Hidenobu Higuchi Masayoshi Chihara Yukana Umemoto Eiji Tanaka Toshiyuki Miyasaka Masayuki Rakugi Hiromi Ogihara Toshio |
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Affiliation: | a Department of Geriatric Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan b Laboratory of Immunodynamics, Department of Microbiology and Immunology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan |
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Abstract: | 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. |
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Keywords: | AoSMC, aortic smooth muscle cells IL-1β, interleukin 1β VSMC, vascular smooth muscle cells NF-κB, nuclear factor κB FITC, fluorescein isothiocyanate FACS, fluorescence-activated cell sorter analysis MFI, mean fluorescence intensity ASA, acetyl salicylic acid |
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