Publications

Detailed Information

Decreased Level and Defective Function of Circulating Endothelial Progenitor Cells in Children With Moyamoya Disease

DC Field Value Language
dc.contributor.authorKim, Jin Hyun-
dc.contributor.authorJung, Ji-Hye-
dc.contributor.authorKang, Hyun-Seung-
dc.contributor.authorPhi, Ji Hoon-
dc.contributor.authorKim, Sang-Jeong-
dc.contributor.authorKim, Young Yim-
dc.contributor.authorWang, Kyu-Chang-
dc.contributor.authorKim, Seung-Ki-
dc.contributor.authorCho, Byung-Kyu-
dc.contributor.authorKim, Young-Hoon-
dc.contributor.authorChae, Jong Hee-
dc.contributor.authorKim, Jeong Eun-
dc.date.accessioned2012-05-22T05:43:23Z-
dc.date.available2012-05-22T05:43:23Z-
dc.date.issued2010-02-15-
dc.identifier.citationJOURNAL OF NEUROSCIENCE RESEARCH; Vol.88 3; 510-518ko_KR
dc.identifier.issn0360-4012-
dc.identifier.urihttps://hdl.handle.net/10371/76231-
dc.description.abstractCirculating endothelial progenitor cells (EPCs) play an important role in physiological and pathological neovascularization and may be involved in attenuating ischemic diseases. This study aimed to characterize circulating EPCs in moyamoya disease (MMD), one of the most common pediatric cerebrovascular diseases. Twenty-eight children with MMD prior to any surgical treatment and 12 healthy volunteers were recruited. Peripheral blood mononuclear cells (PBMNCs) were isolated and cultured in endothelial cell growth medium. Temporal change of phenotype of cells was analyzed on days 0 and 7. The formation of EPC clusters was evaluated on day 7. The CD34(+), CD133(+), and KDR(+) cells, and the number of EPC clusters was significantly reduced in children with MMD. In controls, CD34(+) cells were significantly decreased on day 7 compared with day 0, but in MMD they were only slightly decreased. The change in KDR(+) cells on day 7 compared with day 0 was the reverse of that for CD34(+) cells. Functional assay of EPC demonstrated less tube formation and increased senescent-like phenotype in children with MMD. Analysis of the circulating EPCs of MMD children reveals decreased level and defective function. This study suggests that circulating EPCs may be associated with MMD pathogenesis. (C) 2009 Wiley-Liss, Inc.ko_KR
dc.language.isoenko_KR
dc.publisherWILEY-LISSko_KR
dc.subjectCD34(+) cellsko_KR
dc.subjectendothelial progenitor cellsko_KR
dc.subjectmoyamoya diseaseko_KR
dc.subjectKDR(+) cellsko_KR
dc.subjectclustersko_KR
dc.titleDecreased Level and Defective Function of Circulating Endothelial Progenitor Cells in Children With Moyamoya Diseaseko_KR
dc.typeArticleko_KR
dc.contributor.AlternativeAuthor조병규-
dc.contributor.AlternativeAuthor피지훈-
dc.contributor.AlternativeAuthor김정은-
dc.contributor.AlternativeAuthor김상정-
dc.contributor.AlternativeAuthor김영임-
dc.contributor.AlternativeAuthor김영훈-
dc.contributor.AlternativeAuthor채종희-
dc.contributor.AlternativeAuthor강현승-
dc.contributor.AlternativeAuthor정지혜-
dc.contributor.AlternativeAuthor왕규창-
dc.contributor.AlternativeAuthor김승기-
dc.contributor.AlternativeAuthor김진현-
dc.identifier.doi10.1002/jnr.22228-
dc.citation.journaltitleJOURNAL OF NEUROSCIENCE RESEARCH-
dc.description.citedreferenceWerner N, 2003, CIRC RES, V93, pE17, DOI 10.1161/01.RES.0000083812.30141.74-
dc.description.citedreferenceHeissig B, 2002, CELL, V109, P625-
dc.description.citedreferenceKim SK, 2002, NEUROSURGERY, V50, P88-
dc.description.citedreferenceVasa M, 2001, CIRC RES, V89, pE1-
dc.description.citedreferenceShintani S, 2001, CIRCULATION, V103, P2776-
dc.description.citedreferenceOrlic D, 2001, ANN NY ACAD SCI, V938, P221-
dc.description.citedreferenceTakahashi T, 1999, NAT MED, V5, P434-
dc.description.citedreferenceHojo M, 1998, J NEUROSURG, V89, P623-
dc.description.citedreferenceWakai K, 1997, CLIN NEUROL NEUROSUR, V99, pS1-
dc.description.citedreferenceKim SK, 2003, STROKE, V34, P2835, DOI 10.1161/01.STR.0000100159.43123.D7-
dc.description.citedreferenceHur J, 2004, ARTERIOSCL THROM VAS, V24, P288, DOI 10.1161/01.ATV.0000114236.77009.06-
dc.description.citedreferenceTaguchi A, 2004, CIRCULATION, V109, P2972, DOI 10.1161/01.CIR.0000133311.25587.DE-
dc.description.citedreferenceGhani U, 2005, STROKE, V36, P151, DOI 10.1161/01.STR.0000149944.15406.16-
dc.description.citedreferenceFadini GP, 2005, STROKE, V36, P1112-
dc.description.citedreferenceFukuhra S, 2006, J BIOCHEM MOL BIOL, V39, P132-
dc.description.citedreferenceFadini GP, 2006, STROKE, V37, P2277, DOI 10.1161/01.STR.0000236064.19293.79-
dc.description.citedreferenceShantsila E, 2007, ANN MED, V39, P474, DOI 10.1080/07853890701329283-
dc.description.citedreferenceDunac A, 2007, J NEUROL, V254, P327, DOI 10.1007/s00415-006-0362-1-
dc.description.citedreferenceYOSHIHARA T, 2008, J CEREB BLOOD FLOW M, P1-
dc.description.citedreferenceVestweber D, 2008, ARTERIOSCL THROM VAS, V28, P223, DOI 10.1161/ATVBAHA.107.158014-
dc.description.citedreferenceJung KH, 2008, J CEREBR BLOOD F MET, V28, P1795, DOI 10.1038/jcbfm.2008.67-
dc.description.citedreferenceRafat N, 2009, STROKE, V40, P432, DOI 10.1161/STROKEAHA.108.529420-
dc.description.citedreferenceJie KE, 2009, ATHEROSCLEROSIS, V202, P345, DOI 10.1016/j.atherosclerosis.2008.05.012-
dc.description.citedreferenceMalek AM, 1997, PEDIATR NEUROSURG, V27, P182-
dc.description.citedreferenceAsahara T, 1997, SCIENCE, V275, P964-
dc.description.citedreferenceFukui M, 1997, SURG NEUROL, V47, P138-
dc.description.citedreferenceAOYAGI M, 1993, J CELL PHYSIOL, V154, P281-
dc.description.citedreferenceHOSHIMARU M, 1991, J NEUROSURG, V75, P267-
dc.description.citedreferenceSUZUKI J, 1983, STROKE, V14, P104-
dc.description.tc3-
Appears in Collections:
Files in This Item:
There are no files associated with this item.

Altmetrics

Item View & Download Count

  • mendeley

Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.

Share