Ficolin B in Diabetic Kidney Disease in a Mouse Model of Type 1 Diabetes
Background. The innate immune system may have adverse effects in diabetes and cardiovascular disease. The complement system seems to play a key role through erroneous complement activation via hyperglycaemia-induced neoepitopes. Recently mannan-binding lectin (MBL) was shown to worsen diabetic kidne...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2015/653260 |
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| author | Charlotte Berg Holt Jakob Appel Østergaard Esben Axelgaard Gitte Krogh Nielsen Yuichi Endo Steffen Thiel Troels Krarup Hansen |
| author_facet | Charlotte Berg Holt Jakob Appel Østergaard Esben Axelgaard Gitte Krogh Nielsen Yuichi Endo Steffen Thiel Troels Krarup Hansen |
| author_sort | Charlotte Berg Holt |
| collection | DOAJ |
| description | Background. The innate immune system may have adverse effects in diabetes and cardiovascular disease. The complement system seems to play a key role through erroneous complement activation via hyperglycaemia-induced neoepitopes. Recently mannan-binding lectin (MBL) was shown to worsen diabetic kidney changes. We hypothesize that mouse ficolin B exerts detrimental effects in the diabetic kidney as seen for MBL. Methods. We induced diabetes with streptozotocin in female wild-type mice and ficolin B knockout mice and included two similar nondiabetic groups. Renal hypertrophy and excretion of urinary albumin and creatinine were quantified to assess diabetic kidney damage. Results. In the wild-type groups, the kidney weighed 24% more in the diabetic mice compared to the controls. The diabetes-induced increase in kidney weight was 29% in the ficolin B knockout mice, that is, equal to wild-type animals (two-way ANOVA, P=0.60). In the wild-type mice the albumin-to-creatinine ratio (ACR) was 32.5 mg/g higher in the diabetic mice compared to the controls. The difference was 62.5 mg/g in the ficolin B knockout mice, but this was not significantly different from the wild-type animals (two-way ANOVA, P=0.21). Conclusions. In conclusion, the diabetes-induced effects on kidney weight and ACR were not modified by the presence or absence of ficolin B. |
| format | Article |
| id | doaj-art-fc4dbb616fde4b04a80589f30332d4f7 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
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| series | Mediators of Inflammation |
| spelling | doaj-art-fc4dbb616fde4b04a80589f30332d4f72025-02-03T06:00:43ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/653260653260Ficolin B in Diabetic Kidney Disease in a Mouse Model of Type 1 DiabetesCharlotte Berg Holt0Jakob Appel Østergaard1Esben Axelgaard2Gitte Krogh Nielsen3Yuichi Endo4Steffen Thiel5Troels Krarup Hansen6Department of Endocrinology and Internal Medicine, Aarhus University Hospital, 8000 Aarhus, DenmarkDepartment of Endocrinology and Internal Medicine, Aarhus University Hospital, 8000 Aarhus, DenmarkDepartment of Biomedicine, Aarhus University, 8000 Aarhus, DenmarkDepartment of Biomedicine, Aarhus University, 8000 Aarhus, DenmarkDepartment of Immunology, Fukushima Medical University School of Medicine, Fukushima 960-1295, JapanDepartment of Biomedicine, Aarhus University, 8000 Aarhus, DenmarkDepartment of Endocrinology and Internal Medicine, Aarhus University Hospital, 8000 Aarhus, DenmarkBackground. The innate immune system may have adverse effects in diabetes and cardiovascular disease. The complement system seems to play a key role through erroneous complement activation via hyperglycaemia-induced neoepitopes. Recently mannan-binding lectin (MBL) was shown to worsen diabetic kidney changes. We hypothesize that mouse ficolin B exerts detrimental effects in the diabetic kidney as seen for MBL. Methods. We induced diabetes with streptozotocin in female wild-type mice and ficolin B knockout mice and included two similar nondiabetic groups. Renal hypertrophy and excretion of urinary albumin and creatinine were quantified to assess diabetic kidney damage. Results. In the wild-type groups, the kidney weighed 24% more in the diabetic mice compared to the controls. The diabetes-induced increase in kidney weight was 29% in the ficolin B knockout mice, that is, equal to wild-type animals (two-way ANOVA, P=0.60). In the wild-type mice the albumin-to-creatinine ratio (ACR) was 32.5 mg/g higher in the diabetic mice compared to the controls. The difference was 62.5 mg/g in the ficolin B knockout mice, but this was not significantly different from the wild-type animals (two-way ANOVA, P=0.21). Conclusions. In conclusion, the diabetes-induced effects on kidney weight and ACR were not modified by the presence or absence of ficolin B.http://dx.doi.org/10.1155/2015/653260 |
| spellingShingle | Charlotte Berg Holt Jakob Appel Østergaard Esben Axelgaard Gitte Krogh Nielsen Yuichi Endo Steffen Thiel Troels Krarup Hansen Ficolin B in Diabetic Kidney Disease in a Mouse Model of Type 1 Diabetes Mediators of Inflammation |
| title | Ficolin B in Diabetic Kidney Disease in a Mouse Model of Type 1 Diabetes |
| title_full | Ficolin B in Diabetic Kidney Disease in a Mouse Model of Type 1 Diabetes |
| title_fullStr | Ficolin B in Diabetic Kidney Disease in a Mouse Model of Type 1 Diabetes |
| title_full_unstemmed | Ficolin B in Diabetic Kidney Disease in a Mouse Model of Type 1 Diabetes |
| title_short | Ficolin B in Diabetic Kidney Disease in a Mouse Model of Type 1 Diabetes |
| title_sort | ficolin b in diabetic kidney disease in a mouse model of type 1 diabetes |
| url | http://dx.doi.org/10.1155/2015/653260 |
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