Journal
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
Volume 31, Issue 5, Pages 1075-1083Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/ATVBAHA.111.223545
Keywords
endothelium; gender; leukocytes; nitric oxide; prostacyclin
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Funding
- British Heart Foundation
- Wellcome Trust
- Barts & the London Trustees Basic Science Fellowship
- William Harvey Research Foundation
- National Institute of Health Research
- British Heart Foundation [PG/10/28/28320] Funding Source: researchfish
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Objective-Sex hormones underlie the lower incidence of cardiovascular disease in premenopausal women. Vascular inflammation is involved in the pathogenesis of several cardiovascular diseases and it has been reported that sex hormones modulate inflammatory responses but mechanisms responsible for these effects are not yet fully established. Herein, we assessed whether sex differences in leukocyte recruitment might exist and investigated the underlying mechanisms involved in this response. Methods and Results-Treatment with interleukin-1 beta (IL-1 beta) or tumor necrosis factor-alpha caused leukocyte rolling, adhesion, and emigration in mesenteric postcapillary venules in vivo that was substantially reduced in female mice compared with male mice; this difference was abolished by ovariectomy and partially restored by estrogen replacement. Deletion of endothelial nitric oxide (NO) synthase or cyclooxygenase-1 alone or in combination did not alter the leukocyte recruitment in IL-1 beta-treated females but significantly enhanced this response in male mice. Treatment of murine pulmonary endothelial cells with IL-1 beta increased expression of P-selectin in male but not female cells. Conclusion-We have demonstrated a profound estrogen-dependent and NO and prostacyclin-independent suppression of leukocyte recruitment in females. (Arterioscler Thromb Vasc Biol. 2011;31:1075-1083.)
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