Circulating endothelial cells and vascular injury in systemic lupus erythematosus.

被引：39

作者：

Clancy R.M. ^{[1
]}

机构：

[1] Rheumatology, Hospital for Joint Diseases and New York University School of Medicine, New York

来源：

Current Rheumatology Reports | 2000年 / 2卷 / 1期

关键词：

Nitric Oxide; Systemic Lupus Erythematosus; Systemic Lupus Erythematosus Patient; Sickle Cell Anemia; Thrombotic Thrombocytopenic Purpura;

D O I：

10.1007/s11926-996-0067-6

中图分类号：

学科分类号：

摘要：

In flares of systemic lupus erythematosus (SLE), endothelial cells activated by immune stimuli are potential participants in the inflammatory processes, which contribute to injury. Elevated levels of circulating endothelial cells (CEC) may be a proxy for vascular injury, as demonstrated in patients with sickle cell anemia during acute crises. In active SLE, CEC levels in peripheral blood are elevated (vs healthy controls and correlate with plasma C3a). CEC may reflect widespread unrecognized, ongoing injury despite the absence of clinical stigmata of vasculitis in patients with SLE.

引用

页码：39 / 43

页数：4

共 71 条

[1]

Argenbright LW(1992)Interactions of leukocyte integrins with intercellular adhesion molecule 1 in the production of inflammatory vascular injury in vivo. The Shwartzman reaction revisited J Clin Invest 89 259-272

[2]

Barton RW(1995)Complementmediated regulation of tissue factor activity in endothelium J Exp Med 182 1807-1814

[3]

Saadi S(1995)Identification of C1q as the heat-labile serum cofactor required for immune complexes to stimulate endothelial expression of the adhesion molecules E-selectin and intercellular and vascular cell adhesion molecules 1 Proc Natl Acad Sci U S A 92 8378-8382

[4]

Holzknecht RA(1994)Up-regulation of endothelial cell adhesion molecules characterizes disease activity in systemic lupus erythematosus. The Shwartzman phenomenon revisited Arthritis Rheum 37 376-383

[5]

Patte CP(1992)A mechanism for the antiinflammatory effects of corticosteroids: the glucocorticoid receptor regulates leukocyte adhesion to endothelial cells and expression of endothelial-leukocyte adhesion molecule 1 and intercellular adhesion molecule 1 Proc Natl Acad Sci U S A 89 9991-9995

[6]

Lozada C(1995)Nitric oxide: a novel mediator of inflammation Proc Soc Exp Biol Med 210 93-101

[7]

Levin RI(1997)Increased nitric oxide production accompanied by the up-regulation of inducible nitric oxide synthase in vascular endothelium from patients with systemic lupus erythematosus Arthritis Rheum 40 1810-1816

[8]

Huie M(1994)The role of nitric oxide in the pathogenesis of spontaneous murine autoimmune disease: increased nitric oxide production and nitric oxide synthase expression in MRL-lpr/lpr mice, and reduction of spontaneous glomerulonephritis and arthritis by orally administered NG-monomethyl-L-arginine J Exp Med 179 651-660

[9]

Belmont HM(1997)Clinical and serologic manifestations of autoimmune disease in MRL-lpr/lpr mice lacking nitric oxide synthase type 2 J Exp Med 186 365-373

[10]

Buyon J(1997)Outside-in signaling in the chondrocyte. Nitric oxide disrupts fibronectin-induced assembly of a subplasmalemmal actin/rho A/focal adhesion kinase signaling complex J Clin Invest 100 1789-1796

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