Circulating CD34-positive cells provide an index of cerebrovascular function.
BACKGROUND
Increasing evidence points to a role for circulating endothelial progenitor cells, including populations of CD34- and CD133-positive cells present in peripheral blood, in maintenance of the vasculature and neovascularization. Immature populations, including CD34-positive cells, have been shown to contribute to vascular homeostasis, not only as a pool of endothelial progenitor cells but also as a source of growth/angiogenesis factors at ischemic loci. We hypothesized that diminished numbers of circulating immature cells might impair such physiological and reparative processes, potentially contributing to cerebrovascular dysfunction.


RESULTS
The level of circulating immature cells, CD34-, CD133-, CD117-, and CD135-positive cells, in patients with a history of atherothrombotic cerebral ischemic events was analyzed to assess possible correlations with the degree of carotid atherosclerosis and number of cerebral infarctions. There was a strong inverse correlation between numbers of circulating CD34- and CD133-positive cells and cerebral infarction. In contrast, there was no correlation between the degree of atherosclerosis and populations of circulating immature cells. Analysis of patients with cerebral artery occlusion revealed a significant positive correlation between circulating CD34- and CD133-positive cells and regional blood flow in areas of chronic hypoperfusion.


CONCLUSIONS
These results suggest a possible contribution of circulating CD34- and CD133-positive cells in maintenance of the cerebral circulation in settings of ischemic stress. Our data demonstrate the utility of a simple and precise method to quantify circulating CD34-positive cells, the latter providing a marker of cerebrovascular function.
Taguchi
Akihiko
A
Department of Cerebrovascular Disease, National Cardiovascular Center, 5-7-1 Fujishiro-dai, Suita, Osaka, 565-8565 Japan. ataguchi@res.ncvc.go.jp
Matsuyama
Tomohiro
T
Moriwaki
Hiroshi
H
Hayashi
Takuya
T
Hayashida
Kohei
K
Nagatsuka
Kazuyuki
K
Todo
Kenichi
K
Mori
Katsushi
K
Stern
David M
DM
Soma
Toshihiro
T
Naritomi
Hiroaki
H
D000071916:AC133 Antigen; D000368:Aged; D015703:Antigens, CD; D018952:Antigens, CD34 / Q000032:analysis*; D001772:Blood Cell Count; D002545:Brain Ischemia / Q000097:blood* / Q000209:etiology / Q000503:physiopathology; D002340:Carotid Artery Diseases / Q000097:blood / Q000150:complications / Q000000981:diagnostic imaging; D002454:Cell Differentiation; D002544:Cerebral Infarction / Q000097:blood / Q000150:complications / Q000473:pathology; D002560:Cerebrovascular Circulation; D015897:Comorbidity; D006023:Glycoproteins / Q000032:analysis; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000150:complications; D006973:Hypertension / Q000097:blood / Q000150:complications; D008279:Magnetic Resonance Imaging; D059630:Mesenchymal Stem Cells / Q000502:physiology*; D008875:Middle Aged; D018384:Oxidative Stress; D010455:Peptides / Q000032:analysis; D011518:Proto-Oncogene Proteins / Q000032:analysis; D019009:Proto-Oncogene Proteins c-kit / Q000032:analysis; D020794:Receptor Protein-Tyrosine Kinases / Q000032:analysis; D012038:Regeneration / Q000502:physiology; D016037:Single-Blind Method; D012907:Smoking / Q000097:blood; D014463:Ultrasonography; D051941:fms-Like Tyrosine Kinase 3
D000071916:AC133 Antigen; D015703:Antigens, CD; D018952:Antigens, CD34; D006023:Glycoproteins; C000606023:PROM1 protein, human; D010455:Peptides; D011518:Proto-Oncogene Proteins; C497970:FLT3 protein, human; D019009:Proto-Oncogene Proteins c-kit; D020794:Receptor Protein-Tyrosine Kinases; D051941:fms-Like Tyrosine Kinase 3