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ID 37731
file
creator
Liu, Hong
Mihara, Keiichiro
Kimura, Akiro
Tanaka, Kimio
Kamada, Nanao
subject
Aplastic anemia
Apoptosis
Fas
Serum
NDC
Medical sciences
abstract
To investigate the pathogenesis of aplastic anemia (AA), the apoptosis of CD34+ cells was assayed with annexin V-fluorescein 24hr and 48hr after incubation with the serum of normal controls (n=10), patients with non severe AA (NSAA, n=13) and severe AA (SAA, n=10). The CD34+ progenitors from the bone marrow of normal donors contained a significantly greater proportion of apoptotic cells after incubation with serum from SAA patients than that incubated with serum from normal controls and NSAA. Moreover, the percent apoptosis of CD34+ cells after 24hr incubation with serum from NSAA was slightly higher than that of normal controls. This appears to be related to clinical severity. No significant difference was found in the percent apoptosis of CD34+ cells between incubation for 24hr and 48hr with the same serum. To further explore the mechanism of increased apoptosis induced by the serum of AA patients, the expression of the Fas receptor was measured after incubation with serum from the normal controls and AA patients using flow cytometry. After incubation with serum from the AA patients, the Fas receptor was overexpressed, correlating with the increased apoptosis induced by the same serum from AA patients. In addition, the induction of apoptosis and Fas expression on CD34+ cells by serum from the SAA patients was blocked partly by preincubation of the serum with anti-γ-IFN neutralizing MoAb. These findings suggested that some aberrant components of the serum in the AA patients, which was confirmed partly to be γ-IFN, can induce CD34+ progenitors apoptosis through the Fas signaling pathway. This may contribute to understanding the decreased number of stem cells characteristic of aplastic anemia.
description
This work was supported in part by the Natural Science Foundation of Jiangsu, China (NO. BK97149) and by a grant-in-aid for general scientific research from the Ministry of Education, Science and Culture, Japan (No. 08266109).
journal title
Hiroshima Journal of Medical Sciences
volume
Volume 48
issue
Issue 2
start page
57
end page
63
date of issued
1999-06
publisher
Hiroshima University Medical Press
issn
0018-2052
ncid
language
eng
nii type
Departmental Bulletin Paper
HU type
Departmental Bulletin Papers
DCMI type
text
format
application/pdf
text version
publisher
department
Research Institute for Radiation Biology and Medicine
Graduate School of Biomedical Science
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