ANALYSIS OF CONTRIBUTION OF CYTOKINE AND ITS SIGNAL TRANSDUCTION IN THE PATHOPHYSIOLOGY OF KAWASAKI DISEASE
Project/Area Number |
11670738
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Pediatrics
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Research Institution | GUNMA UNIVERSITY |
Principal Investigator |
ARAKAWA Hirokazu GUNMA UNIVERSITY DEPARTMENT OF PEDIATRICS, GUNMA UNIVERSITY SCHOOL OF MEDICINE, ASSISTANT, 医学部, 助手 (50272232)
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Co-Investigator(Kenkyū-buntansha) |
TAGA Tetsuya GUNMA UNIVERSITY DEPARTMENT OF CELL FATE MODULATION, INSTITUTE OF MOLECULAR EMBRYOLOGY AND GENETICS, KUMAMOTO UNIVERSITY PROFESSOR, 発生医学研究センター・転写制御分野, 教授 (40192629)
森川 昭廣 群馬大学, 医学部, 教授 (40125878)
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Project Period (FY) |
1999 – 2000
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Project Status |
Completed (Fiscal Year 2000)
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Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 2000: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1999: ¥2,500,000 (Direct Cost: ¥2,500,000)
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Keywords | KAWASAKI DISEASE / SIGNAL TRAUSDUCTIONS / GM-CSF / ICAM-1 / TNF-A / HUVEC / GM-CSF / TNF-α / サイトカイン / 赤白血病細胞株 / 細胞内シグナル伝達因子 / STAT |
Research Abstract |
1) We investigate the effect of sera from acute phase of Kawasaki disease on survivals proliferation of Tf-1, a factor-dependent human hemopoietic cell line. TF-1 was incubated with sera from patients in the acute phase of KD for 3 to 5 days. Neither the morphologic change nor survival/proliferation of TF-1 were induced by sera from acute KD, compared with those from control sera or the convalescent phase of KD.However, sera from acute KD.enhanced the proliferation effect of GM-CSF on TF-1. These suggest that there are some factors to enhance GM-CSF effects in the sera from the acute phase of KD.We did not detect any tyrosine phosphorylation of transcription factors, such as STATs (signal transducers and activators of transcription) in TF-1 by incubation with sera from acute KD. 2) We investigate the effect of intercellular adhesion molecule-1 (ICAM-1) and Fas by human umbilical vein endothelial cells (HUVEC). Confluent monolayers of HUVEC were incubated with sera from patients in the acute or convalescent phase of Kawasaki disease. Expression of ICAM-1 and Fas by HUVEC was assessed by flow cytometry. Sera from patients in the acute phase of Kawasaki disease produced significantly greater ICAM-1 expression by HUVEC than sera from patients in the convalescent phase. In contrast, Kawasaki disease did not induce Fas expression. The mean serum concentration of TNF-a in patients in the acute phase of KD was significantly higher than in those in the convalescent phase. Exposure of HUVEC to recombinant human TNF-a increased the expression of both ICAM-1 and Fas. These results suggest that increased expression of ICAM-1 by endothelial cells might be involved in the pathogenesis of acute KD.
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Report
(3 results)
Research Products
(17 results)
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[Publications] Yanagisawa M, Nakashima K, Arakawa H, Ikenaka K, Yoshida K, Kishimoto T, Hisatsune T, Taga T: "Astrocyte differenciation of fetal neuroepithelial cells by interleukin-11 via activation of a common cytokine signal transducer, gp130, and a transcription factor, stat3."J Neurochem. 74. 1494-1504 (2000)
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