|
|
 Previous Article | Table of Contents | Next Article 
Blood, 1 April 2001, Vol. 97, No. 7, pp. 1937-1941
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Modulation of endothelial cell activation in sickle cell disease:
a pilot study
Alex A. Solovey,
Anna N. Solovey,
Jeanne Harkness, and
Robert P. Hebbel
From the Department of Medicine, University of
Minnesota Medical School, Minneapolis.
The vessel wall endothelium undoubtedly plays a role in the
vascular pathobiology of sickle cell disease. This pilot study tested
the feasibility of using an inhibitor of nuclear factor (NF)- B, a
transcription factor, to modify the endothelial activation state
of patients with this vascular disease. For a total of 7 separate
drug exposure tests, 3 subjects with sickle cell disease took
sulfasalazine (given orally at 1 g every 8 hours), and the activation state of their circulating endothelial cells (CECs) was
assessed using immunofluorescence microscopy. Companion studies were
also performed using sulfasalazine in sickle transgenic mice to
verify its effect simultaneously on both CECs and vessel wall endothelium. Both CECs and tissue vessel wall endothelium in sickle mice have an activated phenotype. In these mice sulfasalazine significantly reduced CEC expression of vascular cell adhesion molecule
(VCAM), intracellular adhesion molecule (ICAM), and E-selectin, and it
correspondingly reduced expression of these molecules in some tissue
vessels. In humans with sickle cell disease, sulfasalazine significantly reduced CEC expression of VCAM, ICAM, and E-selectin, but
it did not reduce expression of tissue factor. Addition of a second
transcription factor inhibitor, salsalate, did not change this result.
This pilot study suggests that endothelial cell activation state
can be modified and down-regulated in vivo by sulfasalazine.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
L. De Franceschi, O. S. Platt, G. Malpeli, A. Janin, A. Scarpa, C. Leboeuf, Y. Beuzard, E. Payen, and C. Brugnara
Protective effects of phosphodiesterase-4 (PDE-4) inhibition in the early phase of pulmonary arterial hypertension in transgenic sickle cell mice
FASEB J,
June 1, 2008;
22(6):
1849 - 1860.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Masuda, C. Kalka, T. Takahashi, M. Yoshida, M. Wada, M. Kobori, R. Itoh, H. Iwaguro, M. Eguchi, Y. Iwami, et al.
Estrogen-Mediated Endothelial Progenitor Cell Biology and Kinetics For Physiological Postnatal Vasculogenesis
Circ. Res.,
September 14, 2007;
101(6):
598 - 606.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. J. Telen
Role of Adhesion Molecules and Vascular Endothelium in the Pathogenesis of Sickle Cell Disease
Hematology,
January 1, 2007;
2007(1):
84 - 90.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Buckstein, R. S. Kerbel, Y. Shaked, R. Nayar, C. Foden, R. Turner, C. R. Lee, D. Taylor, L. Zhang, S. Man, et al.
High-Dose Celecoxib and Metronomic "Low-dose" Cyclophosphamide Is an Effective and Safe Therapy in Patients with Relapsed and Refractory Aggressive Histology Non-Hodgkin's Lymphoma
Clin. Cancer Res.,
September 1, 2006;
12(17):
5190 - 5198.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. J. Kato, V. McGowan, R. F. Machado, J. A. Little, J. Taylor VI, C. R. Morris, J. S. Nichols, X. Wang, M. Poljakovic, S. M. Morris Jr, et al.
Lactate dehydrogenase as a biomarker of hemolysis-associated nitric oxide resistance, priapism, leg ulceration, pulmonary hypertension, and death in patients with sickle cell disease
Blood,
March 15, 2006;
107(6):
2279 - 2285.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. W. Lee, G. Y. H. Lip, M. Tayebjee, W. Foster, and A. D. Blann
Circulating endothelial cells, von Willebrand factor, interleukin-6, and prognosis in patients with acute coronary syndromes
Blood,
January 15, 2005;
105(2):
526 - 532.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Solovey, R. Kollander, A. Shet, L. C. Milbauer, S. Choong, A. Panoskaltsis-Mortari, B. R. Blazar, R. J. Kelm Jr, and R. P. Hebbel
Endothelial cell expression of tissue factor in sickle mice is augmented by hypoxia/reoxygenation and inhibited by lovastatin
Blood,
August 1, 2004;
104(3):
840 - 846.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. K. Kaul, X.-d. Liu, S. Choong, J. D. Belcher, G. M. Vercellotti, and R. P. Hebbel
Anti-inflammatory therapy ameliorates leukocyte adhesion and microvascular flow abnormalities in transgenic sickle mice
Am J Physiol Heart Circ Physiol,
July 1, 2004;
287(1):
H293 - H301.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. R. Buchanan, M. R. DeBaun, C. T. Quinn, and M. H. Steinberg
Sickle Cell Disease
Hematology,
January 1, 2004;
2004(1):
35 - 47.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. A. D. T. G. Wagener, H.-D. Volk, D. Willis, N. G. Abraham, M. P. Soares, G. J. Adema, and C. G. Figdor
Different Faces of the Heme-Heme Oxygenase System in Inflammation
Pharmacol. Rev.,
September 1, 2003;
55(3):
551 - 571.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. Perelman, S. K. Selvaraj, S. Batra, L. R. Luck, A. Erdreich-Epstein, T. D. Coates, V. K. Kalra, and P. Malik
Placenta growth factor activates monocytes and correlates with sickle cell disease severity
Blood,
August 15, 2003;
102(4):
1506 - 1514.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. S. Segal, A. Bihorac, and M. Koc
Circulating endothelial cells: tea leaves for renal disease
Am J Physiol Renal Physiol,
July 1, 2002;
283(1):
F11 - F19.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Aslan, T. M. Ryan, B. Adler, T. M. Townes, D. A. Parks, J. A. Thompson, A. Tousson, M. T. Gladwin, R. P. Patel, M. M. Tarpey, et al.
Oxygen radical inhibition of nitric oxide-dependent vascular function in sickle cell disease
PNAS,
December 18, 2001;
98(26):
15215 - 15220.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. N. Y. Setty, A. K. Rao, and M. J. Stuart
Thrombophilia in sickle cell disease: the red cell connection
Blood,
December 1, 2001;
98(12):
3228 - 3233.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Stevens, R. Rosenberg, W. Aird, T. Quertermous, F. L. Johnson, J. G. N. Garcia, R. P. Hebbel, R. M. Tuder, and S. Garfinkel
NHLBI workshop report: endothelial cell phenotypes in heart, lung, and blood diseases
Am J Physiol Cell Physiol,
November 1, 2001;
281(5):
C1422 - C1433.
[Abstract]
[Full Text]
[PDF]
|
|
|
| |
