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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
Cheung, YFChan, SYang, MYe, JYHa, SYWong, SJChan, GCF
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?
DOI: http://dx.doi.org/10.1007/s00277-011-1302-4
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
0939-5555
2021 Impact Factor: 4.030
2020 SCImago Journal Rankings: 1.079
PubMed Central ID
PMC3274669
ISI Accession Number ID
WOS:000300280900004
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

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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.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.en_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.volume91en_US
dc.identifier.issue3en_US
dc.identifier.spage345en_US
dc.identifier.epage352en_US
dc.identifier.eissn1432-0584en_US
dc.identifier.isiWOS:000300280900004-
dc.description.otherSpringer Open Choice, 21 Feb 2012en_US
dc.identifier.scopusauthoridCheung, YF=7202111067-
dc.identifier.scopusauthoridChan, S=35071039700-
dc.identifier.scopusauthoridYang, M=7404927250-
dc.identifier.scopusauthoridYe, JY=23669624100-
dc.identifier.scopusauthoridHa, SY=7202501115-
dc.identifier.scopusauthoridWong, SJ=25924109100-
dc.identifier.scopusauthoridChan, GCF=16160154400-
dc.identifier.citeulike9631716-
dc.identifier.issnl0939-5555-

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