Open AccessCirculating Endothelial Progenitor Cells as a Pathogenetic Marker of Moyamoya Disease
Author(s) -
KeunHwa Jung,
Kon Chu,
Sang Kun Lee,
Hee-Kwon Park,
Dong-Hyun Kim,
Jinhee Kim,
Jae-Jun Bahn,
Eun Kyeung Song,
Manho Kim,
Sang Kun Lee,
Jae-Kyu Roh
Publication year - 2008
Publication title -
journal of cerebral blood flow and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.167
H-Index - 193
eISSN - 1559-7016
pISSN - 0271-678X
DOI - 10.1038/jcbfm.2008.67
Subject(s) - moyamoya disease , matrigel , progenitor cell , vasculogenesis , pathogenesis , medicine , endothelial stem cell , pathology , stem cell , immunology , angiogenesis , biology , in vitro , cancer research , microbiology and biotechnology , biochemistry
Moyamoya disease (MMD) is an unusual form of chronic cerebrovascular occlusive disease that involves the formation of characteristically abnormal vessels. Recent studies have reported that colony-forming unit (CFU) and outgrowth cells represent a subpopulation of endothelial progenitor cells (EPCs). Here, we attempted to determine the significance of CFU number and outgrowth cell yield in MMD. Endothelial progenitor cells were isolated from the blood of 24 adult MMD patients and from 48 age- and risk factor-matched control subjects. After 7 days of culture, CFUs were determined, and yields of outgrowth cells were measured during 2 months of culture. The EPC function was also evaluated using matrigel plate assays. It was found that CFU numbers were significantly lower in MMD patients than in controls. Moreover, during long-term culture, outgrowth cells were isolated from only 10% of control subjects but from 33% of MMD patients, and CFU numbers and tube formation were found to be lower in advanced MMD cases than in those with early stage disease, whereas outgrowth cells were more frequently detected in those with early MMD and moyamoya vessels than in those with advanced disease. These characteristics of circulating EPCs reflect mixed conditions of vascular occlusion and abnormal vasculogenesis during the pathogenesis of MMD.