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Article: Circulating CD133 +VEGFR2 + and CD34 +VEGFR2 + cells and arterial function in patients with beta-thalassaemia major

TitleCirculating CD133 +VEGFR2 + and CD34 +VEGFR2 + cells and arterial function in patients with beta-thalassaemia major
Authors
KeywordsMedicine & Public Health
Hematology
Oncology
Issue Date2011
PublisherSpringer Berlin / Heidelberg
Citation
Annals of Hematology, 2011, v. 91, n. 3, p. 345-352 How to Cite?
AbstractArterial dysfunction has been documented in patients with beta-thalassaemia major. This study aimed to determine the quantity and proliferative capacity of circulating CD133+VEGFR2+ and CD34+VEGFR2+ cells in patients with beta-thalassaemia major and those after haematopoietic stem cell transplantation (HSCT), and their relationships with arterial function. Brachial arterial flow-mediated dilation (FMD), carotid arterial stiffness, the quantity of these circulating cells and their number of colony-forming units (CFUs) were determined in 17 transfusion-dependent thalassaemia patients, 14 patients after HSCT and 11 controls. Compared with controls, both patient groups had significantly lower FMD and greater arterial stiffness. Despite having increased CD133+VEGFR2+ and CD34+VEGFR2+ cells, transfusion-dependent patients had significantly reduced CFUs compared with controls (p = 0.002). There was a trend of increasing CFUs across the three groups with decreasing iron load (p = 0.011). The CFUs correlated with brachial FMD (p = 0.029) and arterial stiffness (p = 0.02), but not with serum ferritin level. Multiple linear regression showed that CFU was a significant determinant of FMD (p = 0.043) and arterial stiffness (p = 0.02) after adjustment of age, sex, body mass index, blood pressure and serum ferritin level. In conclusion, arterial dysfunction found in patients with beta-thalassaemia major before and after HSCT may be related to impaired proliferation of CD133+VEGFR2+ and CD34+VEGFR2+ cells. © 2011 The Author(s).
Persistent Identifierhttp://hdl.handle.net/10722/144928
ISSN
2014 Impact Factor: 2.634
2014 SCImago Journal Rankings: 0.832
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Children's Thalassaemia Foundation
Funding Information:

The authors are grateful to the Children's Thalassaemia Foundation for funding this work

References

Cheung YF, Chan GC, Ha SY (2002) Arterial stiffness and endothelial function in patients with beta-thalassemia major. Circulation 106:2561–2566 doi: 10.1161/01.CIR.0000037225.92759.A7

Gedikli O, Altinbas A, Orucoglu A, Dogan A, Ozaydin M, Aslan SM, Acar G, Canatan D (2007) Elastic properties of the ascending aorta in patients with beta-thalassemia major. Echocardiography 24:830–836 doi: 10.1111/j.1540-8175.2007.00486.x

Ulger Z, Aydinok Y, Gurses D, Levent E, Ozyurek AR (2006) Stiffness of the abdominal aorta in beta-thalassemia major patients related with body iron load. J Pediatr Hematol Oncol 28:647–652 doi: 10.1097/01.mph.0000212987.18694.5a

Cheung YF, Ha SY, Chan GC (2005) Ventriculo-vascular interactions in patients with beta thalassaemia major. Heart 91:769–773 doi: 10.1136/hrt.2003.032110

Cheung YF, Chow PC, Chan GC, Ha SY (2006) Carotid intima–media thickness is increased and related to arterial stiffening in patients with beta-thalassaemia major. Br J Haematol 135:732–734 doi: 10.1111/j.1365-2141.2006.06349.x

Hahalis G, Kremastinos DT, Terzis G, Kalogeropoulos AP, Chrysanthopoulou A, Karakantza M, Kourakli A, Adamopoulos S, Tselepis AD, Grapsas N, Siablis D, Zoumbos NC, Alexopoulos D (2008) Global vasomotor dysfunction and accelerated vascular aging in beta-thalassemia major. Atherosclerosis 198:448–457 doi: 10.1016/j.atherosclerosis.2007.09.030

Kyriakou DS, Alexandrakis MG, Kyriakou ES, Liapi D, Kourelis TV, Passam F, Papadakis A (2001) Activated peripheral blood and endothelial cells in thalassemia patients. Ann Hematol 80:577–583 doi: 10.1007/s002770100355

Rosenzwieg A (2005) Circulation endothelial progenitors—cells as biomarkers. N Engl J Med 353:1055–1056 doi: 10.1056/NEJMe058134

Heiss C, Keymel S, Niesler U, Ziemann J, Kelm M, Kalka C (2005) Impaired progenitor cell activity in age-related endothelial dysfunction. J Am Coll Cardiol 45:1441–1448 doi: 10.1016/j.jacc.2004.12.074

Imanishi T, Hano T, Nishio I (2005) Angiotensin II accelerates endothelial progenitor cell senescence through induction of oxidative stress. J Hypertens 23:97–104 doi: 10.1097/00004872-200501000-00018

Yoder MC (2010) Is endothelium the origin of endothelial progenitor cells? Arterioscler Thromb Vasc Biol 30:1094–1103 doi: 10.1161/ATVBAHA.109.191635

Timmermans F, Plum J, Yöder MC, Ingram DA, Vandekerckhove B, Case J (2009) Endothelial progenitor cells: identity defined? J Cell Mol Med 13:87–102 doi: 10.1111/j.1582-4934.2008.00598.x

Fadini GP, Miorin M, Facco M, Bonamico S, Baesso I, Grego F, Menegolo M, de Kreutzenberg SV, Tiengo A, Agostini C, Avogaro A (2005) Circulating endothelial progenitor cells are reduced in peripheral vascular complications of type 2 diabetes mellitus. J Am Coll Cardiol 45:1449–1457 doi: 10.1016/j.jacc.2004.11.067

Hill JM, Zalos G, Halcox JP, Schenke WH, Waclawiw MA, Quyyumi AA, Finkel T (2003) Circulating endothelial progenitor cells, vascular function, and cardiovascular risk. N Engl J Med 348:593–600 doi: 10.1056/NEJMoa022287

Fadini GP, Coracina A, Baesso I, Agostini C, Tiengo A, Avogaro A, de Kreutzenberg SV (2006) Peripheral blood CD34+KDR+ endothelial progenitor cells are determinants of subclinical atherosclerosis in a middle-aged general population. Stroke 37:2277–2282 doi: 10.1161/01.STR.0000236064.19293.79

Kunz GA, Liang G, Cuculi F, Gregg D, Vata KC, Shaw LK, Goldschmidt-Clermont PJ, Dong C, Taylor DA, Peterson ED (2006) Circulating endothelial progenitor cells predict coronary artery disease severity. Am Heart J 152:190–195 doi: 10.1016/j.ahj.2006.02.001

Werner N, Kosiol S, Schiegl T, Ahlers P, Walenta K, Link A, Bohm M, Nickenig G (2005) Circulating endothelial progenitor cells and cardiovascular outcomes. N Engl J Med 353:999–1007 doi: 10.1056/NEJMoa043814

Aggeli C, Antoniades C, Cosma C, Chrysohoou C, Tousoulis D, Ladis V, Karageorga M, Pitsavos C, Stefanadis C (2005) Endothelial dysfunction and inflammatory process in transfusion-dependent patients with beta-thalassemia major. Int J Cardiol 105:80–84 doi: 10.1016/j.ijcard.2004.12.025

Limsuwan A, Tubtom D, Pakakasama S, Chaunsumrit A (2009) Comparison of vascular complications between conventional treatment and bone marrow transplantation for children with beta-thalassemia disease. Pediatr Cardiol 30:777–780 doi: 10.1007/s00246-009-9436-z

de Witte T (2008) The role of iron in patients after bone marrow transplantation. Blood Rev 22(Suppl 2):S22–S28 doi: 10.1016/S0268-960X(08)70005-5

Evens AM, Mehta J, Gordon LI (2004) Rust and corrosion in hematopoietic stem cell transplantation: the problem of iron and oxidative stress. Bone Marrow Transplant 34:561–571 doi: 10.1038/sj.bmt.1704591

Rodriguez-Crespo I, Nishida CR, Knudsen GM, de Montellano PR (1999) Mutation of the five conserved histidines in the endothelial nitric-oxide synthase hemoprotein domain. No evidence for a non-heme metal requirement for catalysis. J Biol Chem 274:21617–21624 doi: 10.1074/jbc.274.31.21617

Leone AM, Valgimigli M, Giannico MB, Zaccone V, Perfetti M, D’Amario D, Rebuzzi AG, Crea F (2009) From bone marrow to the arterial wall: the ongoing tale of endothelial progenitor cells. Eur Heart J 30:890–899 doi: 10.1093/eurheartj/ehp078

Heeschen C, Aicher A, Lehmann R, Fichtlscherer S, Vasa M, Urbich C, Mildner-Rihm C, Martin H, Zeiher AM, Dimmeler S (2003) Erythropoietin is a potent physiologic stimulus for endothelial progenitor cell mobilization. Blood 102:1340–1346 doi: 10.1182/blood-2003-01-0223

Bahlmann FH, De Groot K, Spandau JM, Landry AL, Hertel B, Duckert T, Boehm SM, Menne J, Haller H, Fliser D (2004) Erythropoietin regulates endothelial progenitor cells. Blood 103:921–926 doi: 10.1182/blood-2003-04-1284

Anning PB, Chen Y, Lamb NJ, Mumby S, Quinlan GJ, Evans TW, Gutteridge JM (1999) Iron overload upregulates haem oxygenase 1 in the lung more rapidly than in other tissues. FEBS Lett 447:111–114 doi: 10.1016/S0014-5793(99)00250-1

Wu BJ, Midwinter RG, Cassano C, Beck K, Wang Y, Changsiri D, Gamble JR, Stocker R (2009) Heme oxygenase-1 increases endothelial progenitor cells. Arterioscler Thromb Vasc Biol 29:1537–1542 doi: 10.1161/ATVBAHA.109.184713

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Tura O, Barclay GR, Roddie H, Davies J, Turner ML (2007) Absence of a relationship between immunophenotypic and colony enumeration analysis of endothelial progenitor cells in clinical haematopoietic cell sources. J Transl Med 5:37 doi: 10.1186/1479-5876-5-37

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Case J, Ingram DA, Haneline LS (2008) Oxidative stress impairs endothelial progenitor cell function. Antioxid Redox Signal 10:1895–1907 doi: 10.1089/ars.2008.2118

He T, Peterson TE, Holmuhamedov EL, Terzic A, Caplice NM, Oberley LW, Katusic ZS (2004) Human endothelial progenitor cells tolerate oxidative stress due to intrinsically high expression of manganese superoxide dismutase. Arterioscler Thromb Vasc Biol 24:2021–2027 doi: 10.1161/01.ATV.0000142810.27849.8f

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DC FieldValueLanguage
dc.contributor.authorCheung, YFen_US
dc.contributor.authorChan, Sen_US
dc.contributor.authorYang, Men_US
dc.contributor.authorYe, JYen_US
dc.contributor.authorHa, SYen_US
dc.contributor.authorWong, SJen_US
dc.contributor.authorChan, GCFen_US
dc.date.accessioned2012-02-21T05:42:57Z-
dc.date.available2012-02-21T05:42:57Z-
dc.date.issued2011en_US
dc.identifier.citationAnnals of Hematology, 2011, v. 91, n. 3, p. 345-352en_US
dc.identifier.issn0939-5555en_US
dc.identifier.urihttp://hdl.handle.net/10722/144928-
dc.description.abstractArterial dysfunction has been documented in patients with beta-thalassaemia major. This study aimed to determine the quantity and proliferative capacity of circulating CD133+VEGFR2+ and CD34+VEGFR2+ cells in patients with beta-thalassaemia major and those after haematopoietic stem cell transplantation (HSCT), and their relationships with arterial function. Brachial arterial flow-mediated dilation (FMD), carotid arterial stiffness, the quantity of these circulating cells and their number of colony-forming units (CFUs) were determined in 17 transfusion-dependent thalassaemia patients, 14 patients after HSCT and 11 controls. Compared with controls, both patient groups had significantly lower FMD and greater arterial stiffness. Despite having increased CD133+VEGFR2+ and CD34+VEGFR2+ cells, transfusion-dependent patients had significantly reduced CFUs compared with controls (p = 0.002). There was a trend of increasing CFUs across the three groups with decreasing iron load (p = 0.011). The CFUs correlated with brachial FMD (p = 0.029) and arterial stiffness (p = 0.02), but not with serum ferritin level. Multiple linear regression showed that CFU was a significant determinant of FMD (p = 0.043) and arterial stiffness (p = 0.02) after adjustment of age, sex, body mass index, blood pressure and serum ferritin level. In conclusion, arterial dysfunction found in patients with beta-thalassaemia major before and after HSCT may be related to impaired proliferation of CD133+VEGFR2+ and CD34+VEGFR2+ cells. © 2011 The Author(s).en_US
dc.languageengen_US
dc.publisherSpringer Berlin / Heidelbergen_US
dc.relation.ispartofAnnals of Hematologyen_US
dc.rightsThe Author(s)en_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong Licenseen_US
dc.subjectMedicine & Public Healthen_US
dc.subjectHematologyen_US
dc.subjectOncologyen_US
dc.titleCirculating CD133 +VEGFR2 + and CD34 +VEGFR2 + cells and arterial function in patients with beta-thalassaemia majoren_US
dc.typeArticleen_US
dc.identifier.openurlhttp://library.hku.hk:4551/resserv?sid=springerlink&genre=article&atitle=Circulating CD133<sup>+</sup>VEGFR2<sup>+</sup> and CD34<sup>+</sup>VEGFR2<sup>+</sup> cells and arterial function in patients with beta-thalassaemia major&title=Annals of Hematology&issn=09395555&date=2012-03-01&volume=91&issue=3& spage=345&authors=Yiu-fai Cheung, Shing Chan, Mo Yang, <i>et al.</i>en_US
dc.identifier.emailCheung, YF:xfcheung@hku.hk-
dc.identifier.emailChan, GCF:gcfchan@hkucc.hku.hk-
dc.identifier.authorityCheung, YF=rp00382-
dc.identifier.authorityChan, GCF=rp00431-
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1007/s00277-011-1302-4en_US
dc.identifier.pmid21808992-
dc.identifier.pmcidPMC3274669-
dc.identifier.scopuseid_2-s2.0-84857363739-
dc.identifier.hkuros191927-
dc.identifier.hkuros198730-
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dc.identifier.spage345en_US
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dc.identifier.eissn1432-0584en_US
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dc.description.otherSpringer Open Choice, 21 Feb 2012en_US
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