期刊
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
卷 27, 期 9, 页码 1998-2004出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/ATVBAHA.107.146449
关键词
T-lymphocytes; interferon-gamma; hypercholesterolemia; endothelial dysfunction; platelets
资金
- NHLBI NIH HHS [HL26441] Funding Source: Medline
Objectives - T-lymphocytes and interferon-gamma (IFN-gamma) contribute to leukocyte recruitment in postcapillary venules during hypercholesterolemia. Our objectives were to determine whether: (1) T-lymphocytes are the source of this IFN-gamma, and (2) whether T-cell-derived IFN-gamma also mediates the accompanying arteriolar dysfunction and platelet adhesion. Methods and Results - Intravital videomicroscopy was used to quantify arteriolar responses to acetylcholine, and leukocyte and platelet adhesion in postcapillary venules of wild-type (WT), immunodeficient (SCID), and IFN-gamma(-/-) mice on a normal (ND) or high-cholesterol (HC) diet. Acetylcholine-induced arteriolar dilation was impaired in WT-HC, compared with WT-ND. This endothelial dysfunction was absent in SCID-HC or IFN-gamma(-/-)-HC mice. Vasodilation was impaired by transfer of WT, but not IFN-gamma(-/-), T-cells to these immunodeficient mice. WT-HC mice exhibited elevated leukocyte and platelet adhesion in venules, versus WT-ND. This blood cell recruitment was attenuated to ND levels in SCID-HC and IFN-gamma(-/-)-HC mice, but restored to WT-HC levels by transfer of WT, but not IFN-gamma(-/-), T-lymphocytes. Conclusions - These data reveal a novel role of T-lymphocyte-derived IFN-gamma in the development of endothelial dysfunction in arterioles during hypercholesterolemia and extend our previous observations that IFN-gamma mediates both inflammatory and thrombogenic responses to hypercholesterolemia in postcapillary venules.
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