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Increased circulating activated endothelial cells, vascular endothelial growth factor, and tumor necrosis factor in thalassemia
Author(s) -
Butthep Punnee,
Rummavas Saknarong,
Wisedpanichkij Raewadee,
Jindadamrongwech Sumalee,
Fucharoen Suthat,
Bunyaratvej Ahd
Publication year - 2002
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.10101
Subject(s) - e selectin , thalassemia , tumor necrosis factor alpha , vascular endothelial growth factor , endothelial stem cell , cell adhesion molecule , medicine , endothelial activation , endocrinology , endothelium , immunology , microbiology and biotechnology , cell , cell adhesion , biology , vegf receptors , biochemistry , in vitro
An increased number of circulating endothelial cells (CECs) was demonstrated in α‐ and β‐thalassemic patients, β‐thalassemia/hemoglobin E (BE), both splenectomized (BE[S]) and non‐splenectomized (BE[NS]), had higher numbers of CECs than α‐thalassemia, both HbH (α‐thal l/α‐thal 2; H) and HbH with hemoglobin Constant Spring (α‐thal 1/CS; H/CS). CECs were also increased in heterozygous HbE (EA) and homozygous HbE (EE). The highest level of tumor necrosis factor‐α (TNF‐α) was found in HbH/CS patients, whereas the highest levels of vascular endothelial growth factor (VEGF) was observed in BE[S] patients. Significant decreases, in protein C and protein S levels were found in both α‐ and β‐thalassemia compared with normal. Good correlations between the numbers of CEC and TNF‐α, VEGF, protein C, and protein S levels were demonstrated in this study. In addition, markers for endothelial cell activation and injury (intercellular adhesion molecule‐1, ICAM‐1/CD54; vascular cell adhesion molecule‐1, VCAM‐1/CD106; and E‐selectin, ELAM‐1/CD62E) were detected on the surface of isolated CECs using immunofluorescence technique. Appearance of CECs with markers for endothelial cell activation, together with increased levels of TNF‐α and VEGF and decreased levels of protein C and protein S in the circulation, may account for the propensity of vascular perturbation in thalassemic subjects. Am. J. Hematol. 70:100–106, 2002. © 2002 Wiley‐Liss, Inc.