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Mannan-Binding Lectin in Diabetic Kidney Disease: The Impact of Mouse Genetics in a Type 1 Diabetes Model
Background. Mannan-binding lectin (MBL) is involved in the development of diabetic nephropathy. MBL is a part of the innate immune system where it can activate the complement system. Serum MBL level predicts later renal impairment in diabetes patients. Direct involvement of MBL in the development of...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3356895/ https://www.ncbi.nlm.nih.gov/pubmed/22645604 http://dx.doi.org/10.1155/2012/678381 |
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author | Østergaard, Jakob Appel Bjerre, Mette RamachandraRao, Satish Posettihalli Sharma, Kumar Nyengaard, Jens Randel Hansen, Troels Krarup Thiel, Steffen Flyvbjerg, Allan |
author_facet | Østergaard, Jakob Appel Bjerre, Mette RamachandraRao, Satish Posettihalli Sharma, Kumar Nyengaard, Jens Randel Hansen, Troels Krarup Thiel, Steffen Flyvbjerg, Allan |
author_sort | Østergaard, Jakob Appel |
collection | PubMed |
description | Background. Mannan-binding lectin (MBL) is involved in the development of diabetic nephropathy. MBL is a part of the innate immune system where it can activate the complement system. Serum MBL level predicts later renal impairment in diabetes patients. Direct involvement of MBL in the development of diabetic kidney disease is observed in one animal strain. However, this involvement may differ among the animal strains. We thus examined the impact of the genetic background on the role of MBL in diabetic nephropathy. Materials/Methods. C57BL/6JBomTac and 129S6/SvEvTac mice were compared. In both strains, experimental type 1 diabetes was induced in wild-type (WT) and MBL-knockout (MBL-KO) mice by streptozotocin. Nondiabetic WT and MBL-KO mice were used as controls. We tested if MBL modified the diabetes-induced kidney changes by two-way ANOVA allowing for interaction. Results. MBL aggravated diabetes-induced kidney growth and glomerulus enlargement in C57BL/6JBomTac mice. MBL did not modify diabetes effects on glomerular basement membrane thickness or mesangial volume in any strain. Diabetes-induced changes in renal gene transcription of growth factors and matrix components were unaffected by MBL. Conclusions. Strain-specific MBL effects were found on downstream diabetic kidney changes. This emphasizes the importance of genetic background in this model of diabetic complications. |
format | Online Article Text |
id | pubmed-3356895 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-33568952012-05-29 Mannan-Binding Lectin in Diabetic Kidney Disease: The Impact of Mouse Genetics in a Type 1 Diabetes Model Østergaard, Jakob Appel Bjerre, Mette RamachandraRao, Satish Posettihalli Sharma, Kumar Nyengaard, Jens Randel Hansen, Troels Krarup Thiel, Steffen Flyvbjerg, Allan Exp Diabetes Res Research Article Background. Mannan-binding lectin (MBL) is involved in the development of diabetic nephropathy. MBL is a part of the innate immune system where it can activate the complement system. Serum MBL level predicts later renal impairment in diabetes patients. Direct involvement of MBL in the development of diabetic kidney disease is observed in one animal strain. However, this involvement may differ among the animal strains. We thus examined the impact of the genetic background on the role of MBL in diabetic nephropathy. Materials/Methods. C57BL/6JBomTac and 129S6/SvEvTac mice were compared. In both strains, experimental type 1 diabetes was induced in wild-type (WT) and MBL-knockout (MBL-KO) mice by streptozotocin. Nondiabetic WT and MBL-KO mice were used as controls. We tested if MBL modified the diabetes-induced kidney changes by two-way ANOVA allowing for interaction. Results. MBL aggravated diabetes-induced kidney growth and glomerulus enlargement in C57BL/6JBomTac mice. MBL did not modify diabetes effects on glomerular basement membrane thickness or mesangial volume in any strain. Diabetes-induced changes in renal gene transcription of growth factors and matrix components were unaffected by MBL. Conclusions. Strain-specific MBL effects were found on downstream diabetic kidney changes. This emphasizes the importance of genetic background in this model of diabetic complications. Hindawi Publishing Corporation 2012 2012-05-08 /pmc/articles/PMC3356895/ /pubmed/22645604 http://dx.doi.org/10.1155/2012/678381 Text en Copyright © 2012 Jakob Appel Østergaard et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Østergaard, Jakob Appel Bjerre, Mette RamachandraRao, Satish Posettihalli Sharma, Kumar Nyengaard, Jens Randel Hansen, Troels Krarup Thiel, Steffen Flyvbjerg, Allan Mannan-Binding Lectin in Diabetic Kidney Disease: The Impact of Mouse Genetics in a Type 1 Diabetes Model |
title | Mannan-Binding Lectin in Diabetic Kidney Disease: The Impact of Mouse Genetics in a Type 1 Diabetes Model |
title_full | Mannan-Binding Lectin in Diabetic Kidney Disease: The Impact of Mouse Genetics in a Type 1 Diabetes Model |
title_fullStr | Mannan-Binding Lectin in Diabetic Kidney Disease: The Impact of Mouse Genetics in a Type 1 Diabetes Model |
title_full_unstemmed | Mannan-Binding Lectin in Diabetic Kidney Disease: The Impact of Mouse Genetics in a Type 1 Diabetes Model |
title_short | Mannan-Binding Lectin in Diabetic Kidney Disease: The Impact of Mouse Genetics in a Type 1 Diabetes Model |
title_sort | mannan-binding lectin in diabetic kidney disease: the impact of mouse genetics in a type 1 diabetes model |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3356895/ https://www.ncbi.nlm.nih.gov/pubmed/22645604 http://dx.doi.org/10.1155/2012/678381 |
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