help button home button
AJRCCM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by HAMMERMAN, S. I.
Right arrow Articles by FARBER, H. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by HAMMERMAN, S. I.
Right arrow Articles by FARBER, H. W.

Am. J. Respir. Crit. Care Med., Volume 156, Number 1, July 1997, 280-285

Endothelin-1 Production during the Acute Chest Syndrome in Sickle Cell Disease

SAMUEL I. HAMMERMAN, STELLA KOUREMBANAS, TAMMY J. CONCA, MARISA TUCCI, MARK BRAUER, and HARRISON W. FARBER

Pulmonary Center and Division of Hematology, Boston University School of Medicine, Boston; Joint Program in Neonatology, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts

To investigate the role of the endothelial-derived vasoactive mediator endothelin (ET-1) in the acute chest syndrome (ACS), we incubated bovine pulmonary artery endothelial cells (BPAEC) with red blood cells (equivalent to a hematocrit of 20%) and/or autologous plasma (1:10 dilution) from two patients during ACS and during routine clinic visits. Cellular RNA was analyzed for ET-1 transcripts by Northern analysis and ET-1 protein levels in BPAEC supernatants and in plasma measured by radioimmunoassay. ET-1 mRNA expression and protein levels increased in BPAEC exposed to plasma obtained during ACS; in contrast, exposure to plasma obtained during routine clinic visits did not alter BPAEC ET-1 mRNA expression or protein levels. Plasma ET-1 level was elevated during ACS, decreased during resolution, and remained slightly elevated during routine clinic visits. Plasma obtained from one patient 4 d prior to hospitalization for vasoocclusive crisis contained the highest ET-1 level and markedly increased BPAEC ET-1 mRNA expression and protein levels. In both patients, BPAEC ET-1 mRNA and protein expression in vitro and plasma ET-1 levels in vivo correlated with stage of disease and occurred in the absence of direct erythrocyte contact in vitro. These observations suggest that ET-1 production contributes to development of ACS.




This article has been cited by other articles:


Home page
 BloodHome page
N. Patel, C. S. Gonsalves, P. Malik, and V. K. Kalra
Placenta growth factor augments endothelin-1 and endothelin-B receptor expression via hypoxia-inducible factor-1{alpha}
Blood, August 1, 2008; 112(3): 856 - 865.
[Abstract] [Full Text] [PDF]

Home page
 FASEB J.Home page
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]

Home page
 haematolHome page
K. I. Ataga, C. G. Moore, C. A. Hillery, S. Jones, H. C. Whinna, D. Strayhorn, C. Sohier, A. Hinderliter, L. V. Parise, and E. P. Orringer
Coagulation activation and inflammation in sickle cell disease-associated pulmonary hypertension
Haematologica, January 1, 2008; 93(1): 20 - 26.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
A. Rivera
Reduced sickle erythrocyte dehydration in vivo by endothelin-1 receptor antagonists
Am J Physiol Cell Physiol, September 1, 2007; 293(3): C960 - C966.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. GenomicsHome page
E. S. Klings, S. Safaya, A. H. Adewoye, A. Odhiambo, G. Frampton, M. Lenburg, N. Gerry, P. Sebastiani, M. H. Steinberg, and H. W. Farber
Differential gene expression in pulmonary artery endothelial cells exposed to sickle cell plasma
Physiol Genomics, May 11, 2005; 21(3): 293 - 298.
[Abstract] [Full Text] [PDF]

Home page
 ASH Education BookHome page
M. T. Gladwin and G. J. Kato
Cardiopulmonary Complications of Sickle Cell Disease: Role of Nitric Oxide and Hemolytic Anemia
Hematology, January 1, 2005; 2005(1): 51 - 57.
[Abstract] [Full Text] [PDF]

Home page
 NEJMHome page
E. S. Klings, H. W. Farber, P. M. Hassoun, J. A. Krishnan, M. T. Gladwin, V. Sachdev, and F. P. Ognibene
Pulmonary Hypertension as a Risk Factor for Death in Patients with Sickle Cell Disease
N. Engl. J. Med., June 10, 2004; 350(24): 2521 - 2522.
[Full Text] [PDF]

Home page
 NEJMHome page
M. T. Gladwin, V. Sachdev, M. L. Jison, Y. Shizukuda, J. F. Plehn, K. Minter, B. Brown, W. A. Coles, J. S. Nichols, I. Ernst, et al.
Pulmonary Hypertension as a Risk Factor for Death in Patients with Sickle Cell Disease
N. Engl. J. Med., February 26, 2004; 350(9): 886 - 895.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
E. Lechapt, A. Habibi, D. Bachir, F. Galacteros, A. Schaeffer, D. Desvaux, L. Brochard, B. Housset, B. Godeau, and B. Maitre
Induced Sputum versus Bronchoalveolar Lavage during Acute Chest Syndrome in Sickle Cell Disease
Am. J. Respir. Crit. Care Med., December 1, 2003; 168(11): 1373 - 1377.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
C. R. Morris, S. M. Morris Jr., W. Hagar, J. van Warmerdam, S. Claster, D. Kepka-Lenhart, L. Machado, F. A. Kuypers, and E. P. Vichinsky
Arginine Therapy: A New Treatment for Pulmonary Hypertension in Sickle Cell Disease?
Am. J. Respir. Crit. Care Med., July 1, 2003; 168(1): 63 - 69.
[Abstract] [Full Text] [PDF]

Home page
 Postgrad. Med. J.Home page
A K Siddiqui and S Ahmed
Pulmonary manifestations of sickle cell disease
Postgrad. Med. J., July 1, 2003; 79(933): 384 - 390.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
J. D. Belcher, C. J. Bryant, J. Nguyen, P. R. Bowlin, M. C. Kielbik, J. C. Bischof, R. P. Hebbel, and G. M. Vercellotti
Transgenic sickle mice have vascular inflammation
Blood, May 15, 2003; 101(10): 3953 - 3959.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
A. Khodorova, M. U. Fareed, A. Gokin, G. R. Strichartz, and G. Davar
Local Injection of a Selective Endothelin-B Receptor Agonist Inhibits Endothelin-1-Induced Pain-Like Behavior and Excitation of Nociceptors in a Naloxone-Sensitive Manner
J. Neurosci., September 1, 2002; 22(17): 7788 - 7796.
[Abstract] [Full Text] [PDF]

Home page
 ChestHome page
S. H. Salzman
Does Splinting From Thoracic Bone Ischemia and Infarction Contribute to the Acute Chest Syndrome in Sickle Cell Disease?
Chest, July 1, 2002; 122(1): 6 - 9.
[Full Text] [PDF]

Home page
 ASH Education BookHome page
M. C. Walters, A. W. Nienhuis, and E. Vichinsky
Novel Therapeutic Approaches in Sickle Cell Disease
Hematology, January 1, 2002; 2002(1): 10 - 34.
[Abstract] [Full Text]

Home page
 Am. J. Respir. Crit. Care Med.Home page
E. S. KLINGS, B. W. CHRISTMAN, J. MCCLUNG, A. F. STUCCHI, L. MCMAHON, M. BRAUER, and H. W. FARBER
Increased F2 Isoprostanes in the Acute Chest Syndrome of Sickle Cell Disease as a Marker of Oxidative Stress
Am. J. Respir. Crit. Care Med., October 1, 2001; 164(7): 1248 - 1252.
[Abstract] [Full Text] [PDF]

Home page
 ChestHome page
C. Moser, E. Nussbaum, and D. M. Cooper
Plastic Bronchitis and the Role of Bronchoscopy in the Acute Chest Syndrome of Sickle Cell Disease
Chest, August 1, 2001; 120(2): 608 - 613.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
A. P. Gokin, M. U. Fareed, H.-L. Pan, G. Hans, G. R. Strichartz, and G. Davar
Local Injection of Endothelin-1 Produces Pain-Like Behavior and Excitation of Nociceptors in Rats
J. Neurosci., July 15, 2001; 21(14): 5358 - 5366.
[Abstract] [Full Text] [PDF]

Home page
 Ann. N. Y. Acad. Sci.Home page
M. ASLAN, D. THORNLEY-BROWN, and B. A. FREEMAN
Reactive Species in Sickle Cell Disease
Ann. N.Y. Acad. Sci., January 1, 2000; 899(1): 375 - 391.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
A. Rivera, M. A. Rotter, and C. Brugnara
Endothelins activate Ca2+-gated K+ channels via endothelin B receptors in CD-1 mouse erythrocytes
Am J Physiol Cell Physiol, October 1, 1999; 277(4): C746 - C754.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
S. I. Hammerman, E. S. Klings, K. P. Hendra, G. R. Upchurch Jr., D. C. Rishikof, J. Loscalzo, and H. W. Farber
Endothelial cell nitric oxide production in acute chest syndrome
Am J Physiol Heart Circ Physiol, October 1, 1999; 277(4): H1579 - H1592.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
M. J. Stuart and B.N. Y. Setty
Sickle Cell Acute Chest Syndrome: Pathogenesis and Rationale for Treatment
Blood, September 1, 1999; 94(5): 1555 - 1560.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
M. T. GLADWIN, A. N. SCHECHTER, J. H. SHELHAMER, and F. P. OGNIBENE
The Acute Chest Syndrome in Sickle Cell Disease . Possible Role of Nitric Oxide in Its Pathophysiology and Treatment
Am. J. Respir. Crit. Care Med., May 1, 1999; 159(5): 1368 - 1376.
[Full Text] [PDF]

Home page
 BloodHome page
E. Graido-Gonzalez, J. C. Doherty, E. W. Bergreen, G. Organ, M. Telfer, and M. A. McMillen
Plasma Endothelin-1, Cytokine, and Prostaglandin E2 Levels in Sickle Cell Disease and Acute Vaso-Occlusive Sickle Crisis
Blood, October 1, 1998; 92(7): 2551 - 2555.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 1997 American Thoracic Society