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Interleukin-10 Promoter Polymorphism is Associated with the Predisposition to the Development of IgA Nephropathy and Focal Segmental Glomerulosclerosis in Korea
The roles of interleukin-10 (IL-10) have been emphasized in several models of glomerulonephritis (GN). Three biallelic polymorphisms within the IL-10 promoter region, at positions -1,082, -819, and -592 from the transcription initiation site, were shown to affect the level of IL-10 production. To in...
Autores principales: | , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Korean Academy of Medical Sciences
2005
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2779332/ https://www.ncbi.nlm.nih.gov/pubmed/16361810 http://dx.doi.org/10.3346/jkms.2005.20.6.989 |
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author | Chin, Ho Jun Na, Ki Young Kim, Soo Jin Oh, Kook-Hwan Kim, Yon Su Lim, Chun Soo Kim, Suhnggwon Chae, Dong-Wan |
author_facet | Chin, Ho Jun Na, Ki Young Kim, Soo Jin Oh, Kook-Hwan Kim, Yon Su Lim, Chun Soo Kim, Suhnggwon Chae, Dong-Wan |
author_sort | Chin, Ho Jun |
collection | PubMed |
description | The roles of interleukin-10 (IL-10) have been emphasized in several models of glomerulonephritis (GN). Three biallelic polymorphisms within the IL-10 promoter region, at positions -1,082, -819, and -592 from the transcription initiation site, were shown to affect the level of IL-10 production. To investigate the effect of IL-10 promoter polymorphisms on the predisposition to development of GN in Korea, IL-10 promoter polymorphisms were assayed by polymerase chain reaction followed by restriction fragment length polymorphism in 108 patients with IgA nephropathy (IgAN), 49 focal segmental glomerulosclerosis (FSGS), and 100 healthy controls. In comparison with the control, the frequency of -1,082*G alleles were lower in IgAN and the frequencies of -592*C and -819*C were lower in FSGS, respectively. As for the haplotype, GCC haplotype was less frequent among IgAN than the control and ATA haplotype was more frequent among FSGS than the control (p<0.05). The frequency of intermediate producer genotypes (GCC/ACC and GCC/ATA) were lower among IgAN or FSGS than the control. Our findings suggested that IL-10 promoter polymorphism predisposed to the development of IgAN and FSGS in Korean patients. |
format | Text |
id | pubmed-2779332 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2005 |
publisher | The Korean Academy of Medical Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-27793322009-11-20 Interleukin-10 Promoter Polymorphism is Associated with the Predisposition to the Development of IgA Nephropathy and Focal Segmental Glomerulosclerosis in Korea Chin, Ho Jun Na, Ki Young Kim, Soo Jin Oh, Kook-Hwan Kim, Yon Su Lim, Chun Soo Kim, Suhnggwon Chae, Dong-Wan J Korean Med Sci Original Article The roles of interleukin-10 (IL-10) have been emphasized in several models of glomerulonephritis (GN). Three biallelic polymorphisms within the IL-10 promoter region, at positions -1,082, -819, and -592 from the transcription initiation site, were shown to affect the level of IL-10 production. To investigate the effect of IL-10 promoter polymorphisms on the predisposition to development of GN in Korea, IL-10 promoter polymorphisms were assayed by polymerase chain reaction followed by restriction fragment length polymorphism in 108 patients with IgA nephropathy (IgAN), 49 focal segmental glomerulosclerosis (FSGS), and 100 healthy controls. In comparison with the control, the frequency of -1,082*G alleles were lower in IgAN and the frequencies of -592*C and -819*C were lower in FSGS, respectively. As for the haplotype, GCC haplotype was less frequent among IgAN than the control and ATA haplotype was more frequent among FSGS than the control (p<0.05). The frequency of intermediate producer genotypes (GCC/ACC and GCC/ATA) were lower among IgAN or FSGS than the control. Our findings suggested that IL-10 promoter polymorphism predisposed to the development of IgAN and FSGS in Korean patients. The Korean Academy of Medical Sciences 2005-12 2005-12-31 /pmc/articles/PMC2779332/ /pubmed/16361810 http://dx.doi.org/10.3346/jkms.2005.20.6.989 Text en Copyright © 2005 The Korean Academy of Medical Sciences http://creativecommons.org/licenses/by-nc/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Chin, Ho Jun Na, Ki Young Kim, Soo Jin Oh, Kook-Hwan Kim, Yon Su Lim, Chun Soo Kim, Suhnggwon Chae, Dong-Wan Interleukin-10 Promoter Polymorphism is Associated with the Predisposition to the Development of IgA Nephropathy and Focal Segmental Glomerulosclerosis in Korea |
title | Interleukin-10 Promoter Polymorphism is Associated with the Predisposition to the Development of IgA Nephropathy and Focal Segmental Glomerulosclerosis in Korea |
title_full | Interleukin-10 Promoter Polymorphism is Associated with the Predisposition to the Development of IgA Nephropathy and Focal Segmental Glomerulosclerosis in Korea |
title_fullStr | Interleukin-10 Promoter Polymorphism is Associated with the Predisposition to the Development of IgA Nephropathy and Focal Segmental Glomerulosclerosis in Korea |
title_full_unstemmed | Interleukin-10 Promoter Polymorphism is Associated with the Predisposition to the Development of IgA Nephropathy and Focal Segmental Glomerulosclerosis in Korea |
title_short | Interleukin-10 Promoter Polymorphism is Associated with the Predisposition to the Development of IgA Nephropathy and Focal Segmental Glomerulosclerosis in Korea |
title_sort | interleukin-10 promoter polymorphism is associated with the predisposition to the development of iga nephropathy and focal segmental glomerulosclerosis in korea |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2779332/ https://www.ncbi.nlm.nih.gov/pubmed/16361810 http://dx.doi.org/10.3346/jkms.2005.20.6.989 |
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