2003 Fiscal Year Final Research Report Summary
Pathogenesis of Kawasaki disease : Gene expression in susceptible hosts determined by microarray
Project/Area Number |
14570786
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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 | KURUME UNIVERSITY |
Principal Investigator |
ISHII Masahiro Kurume University, Assistant Professor, 医学部, 講師 (90222950)
|
Co-Investigator(Kenkyū-buntansha) |
SUGAHARA Yoko Kurume University, Fellow, 医学部, 助手 (40309787)
FURUI Jun Kurume University, Fellow, 医学部, 助手 (00341339)
MUTA Hiromi Kurume University, Fellow, 医学部, 助手 (40343694)
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Project Period (FY) |
2002 – 2003
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Keywords | Kawasaki disease / Pathogenesis / Gene expression / Coronary artery lesion / Vasuculitis / Gene chip / 細胞接着分子 / 血管新生因子 |
Research Abstract |
Background : The etiology of Kawasaki disease (KD) remains unknown despite extensive investigations. Our hypothesis suggested that very common infectious agents might cause KD in some susceptible hosts. We investigated the difference of gene expression between patients with KD and control subjects by use the Affymetrix GeneChip system. Methods : Five patients with KD, ranged age from to years, mean follow up periods years, including Group A patients (n=8) who had coronary artery lesions GALs and Group B patients (n=8) who had no GALs, 2 patients who had no history of KD as controls (n=10), were studied. We analyzed a gene expression profile with RNA sample provided mononuclear cells in peripheral white blood cells. The difference of gene expression did more than 1.5 times with significance. Result : Most gene expression in KD patients was resembled. However some differences of gene expression were found among 3 groups. The gene of Human gremline IgD chain gene and H.sapiens mRNA for T
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cell lerkemia/lymphoma 1 were expressed on KD patients with CALs more than on patients with no CALs. In addition, the gene of Homo sapiens mRNA for KIAA0752 protein were expressed on KD patients with GALS more than on KD patients with no CALS. The connection gene of a Human MHC class II HLA-DR7 and Human MHC class II I-ILA-DRw53 were expressed on KD patients with GALS more than patients who had no history of KD. The gene of Human complement cytolysis inhibitor (CLI) mRNA and Spermidine/Spermine N1-Acetyltransferase (SS-A) were expression on patients without history of KD more than KD patients with CALs. SS-A gene may relate to vascular disease. Previous report suggested that gene expression of the SS-A related to the shear stress in human umbilical vein endothelial cells. Conclusion : This study suggested that some hereditary factors may participate in KD patients, especially to relate the factors of vascular disease. The present results demonstrate the merit of further investigation of the alterations as a source of baseline information for the design of future genetic therapy for coronary artery lesions due to KD vasculitis. Less
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Research Products
(10 results)