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Transcriptomic Analysis in Diabetic Nephropathy of Streptozotocin-Induced Diabetic Rats
Diabetic nephropathy (DN) is a major complication of diabetes and is caused by an imbalance in the expression of certain genes that activate or inhibit vital cellular functions of kidney. Despite several recent advances, the pathogenesis of DN remains far from clear, suggesting the need to carry out...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Molecular Diversity Preservation International (MDPI)
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257079/ https://www.ncbi.nlm.nih.gov/pubmed/22272082 http://dx.doi.org/10.3390/ijms12128431 |
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author | Lomas-Soria, Consuelo Ramos-Gómez, Minerva Guevara-Olvera, Lorenzo Guevara-González, Ramón Torres-Pacheco, Irineo Gallegos-Corona, Marco A. Reynoso-Camacho, Rosalía |
author_facet | Lomas-Soria, Consuelo Ramos-Gómez, Minerva Guevara-Olvera, Lorenzo Guevara-González, Ramón Torres-Pacheco, Irineo Gallegos-Corona, Marco A. Reynoso-Camacho, Rosalía |
author_sort | Lomas-Soria, Consuelo |
collection | PubMed |
description | Diabetic nephropathy (DN) is a major complication of diabetes and is caused by an imbalance in the expression of certain genes that activate or inhibit vital cellular functions of kidney. Despite several recent advances, the pathogenesis of DN remains far from clear, suggesting the need to carry out studies identifying molecular aspects, such as gene expression, that could play a key role in the development of DN. There are several techniques to analyze transcriptome in living organisms. In this study, the suppression subtractive hybridization (SSH) method was used to generate up- and down-regulated subtracted cDNA libraries in the kidney of streptozotocin (STZ)-induced diabetic rats. Northern-blot analysis was used to confirm differential expression ratios from the obtained SSH clones to identify genes related to DN. 400 unique SSH clones were randomly chosen from the two subtraction libraries (200 of each) and verified as differentially expressed. According to blast screening and functional annotation, 20.2% and 20.9% of genes were related to metabolism proteins, 9% and 3.6% to transporters and channels, 16% and 6.3% to transcription factors, 19% and 17.2% to hypothetical proteins, and finally 24.1 and 17.2% to unknown genes, from the down- and up-regulated libraries, respectively. The down- and up-regulated cDNA libraries differentially expressed in the kidney of STZ diabetic rats have been successfully constructed and some identified genes could be highly important in DN. |
format | Online Article Text |
id | pubmed-3257079 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Molecular Diversity Preservation International (MDPI) |
record_format | MEDLINE/PubMed |
spelling | pubmed-32570792012-01-23 Transcriptomic Analysis in Diabetic Nephropathy of Streptozotocin-Induced Diabetic Rats Lomas-Soria, Consuelo Ramos-Gómez, Minerva Guevara-Olvera, Lorenzo Guevara-González, Ramón Torres-Pacheco, Irineo Gallegos-Corona, Marco A. Reynoso-Camacho, Rosalía Int J Mol Sci Article Diabetic nephropathy (DN) is a major complication of diabetes and is caused by an imbalance in the expression of certain genes that activate or inhibit vital cellular functions of kidney. Despite several recent advances, the pathogenesis of DN remains far from clear, suggesting the need to carry out studies identifying molecular aspects, such as gene expression, that could play a key role in the development of DN. There are several techniques to analyze transcriptome in living organisms. In this study, the suppression subtractive hybridization (SSH) method was used to generate up- and down-regulated subtracted cDNA libraries in the kidney of streptozotocin (STZ)-induced diabetic rats. Northern-blot analysis was used to confirm differential expression ratios from the obtained SSH clones to identify genes related to DN. 400 unique SSH clones were randomly chosen from the two subtraction libraries (200 of each) and verified as differentially expressed. According to blast screening and functional annotation, 20.2% and 20.9% of genes were related to metabolism proteins, 9% and 3.6% to transporters and channels, 16% and 6.3% to transcription factors, 19% and 17.2% to hypothetical proteins, and finally 24.1 and 17.2% to unknown genes, from the down- and up-regulated libraries, respectively. The down- and up-regulated cDNA libraries differentially expressed in the kidney of STZ diabetic rats have been successfully constructed and some identified genes could be highly important in DN. Molecular Diversity Preservation International (MDPI) 2011-11-29 /pmc/articles/PMC3257079/ /pubmed/22272082 http://dx.doi.org/10.3390/ijms12128431 Text en © 2011 by the authors; licensee MDPI, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0 This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). |
spellingShingle | Article Lomas-Soria, Consuelo Ramos-Gómez, Minerva Guevara-Olvera, Lorenzo Guevara-González, Ramón Torres-Pacheco, Irineo Gallegos-Corona, Marco A. Reynoso-Camacho, Rosalía Transcriptomic Analysis in Diabetic Nephropathy of Streptozotocin-Induced Diabetic Rats |
title | Transcriptomic Analysis in Diabetic Nephropathy of Streptozotocin-Induced Diabetic Rats |
title_full | Transcriptomic Analysis in Diabetic Nephropathy of Streptozotocin-Induced Diabetic Rats |
title_fullStr | Transcriptomic Analysis in Diabetic Nephropathy of Streptozotocin-Induced Diabetic Rats |
title_full_unstemmed | Transcriptomic Analysis in Diabetic Nephropathy of Streptozotocin-Induced Diabetic Rats |
title_short | Transcriptomic Analysis in Diabetic Nephropathy of Streptozotocin-Induced Diabetic Rats |
title_sort | transcriptomic analysis in diabetic nephropathy of streptozotocin-induced diabetic rats |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257079/ https://www.ncbi.nlm.nih.gov/pubmed/22272082 http://dx.doi.org/10.3390/ijms12128431 |
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