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Blood, 15 May 2004, Vol. 103, No. 10, pp. 3677-3683.
Prepublished online as a Blood First Edition Paper on January 15, 2004; DOI 10.1182/blood-2003-09-3198.
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CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Endothelial cell apoptosis in systemic lupus erythematosus: a common pathway for abnormal vascular function and thrombosis propensity
Sanjay Rajagopalan,
Emily C. Somers,
Robert D. Brook,
Christine Kehrer,
Dana Pfenninger,
Emily Lewis,
Anjan Chakrabarti,
Bruce C. Richardson,
Eric Shelden,
W. Joseph McCune, and
Mariana J. Kaplan
From the Divisions of Cardiology and Rheumatology, and the Department of Cell and Developmental Biology, University of Michigan, Ann Arbor.
Women with systemic lupus erythematosus (SLE) are at risk for premature atherothrombosis independent of Framingham risk factors. We investigated whether endothelial cell (EC) apoptosis predicts abnormal vasomotor tone and contributes to circulating tissue factor (TF) levels in this disease. Brachial artery flow-mediated dilation (FMD) and nitroglycerin-mediated dilation were determined in women with SLE, healthy control subjects, and subjects with coronary artery disease (CAD) (n = 43/group). Quantification of circulating apoptotic ECs was performed by flow cytometry (CD146+ cells that stained for Annexin V [CD146AnnV+]) and immunofluorescent microscopy. Plasma TF was measured by enzyme-linked immunosorbent assay (ELISA). Compared with healthy control and CAD subjects, patients with SLE had higher numbers of circulating CD146AnnV+ cells (10 ± 3, 18 ± 5, and 89 ± 32 cells/mL, respectively, mean ± SEM; P < .01). Increased CD146AnnV+ cells correlated strongly with abnormal vascular function (P = .037). After adjusting for known predictors of endothelial function, CD146AnnV+ was the only variable that predicted FMD ( = –4.5, P < .001). Increased CD146AnnV+ was strongly associated with elevated levels of circulating TF (r = .46, P = .002). Circulating apoptotic ECs are elevated in young women with SLE and strongly correlate with markedly abnormal vascular function and elevated TF levels. Heightened endothelial apoptosis may represent an important mechanism for development of atherothrombosis in SLE.
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