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Ficolin B in Diabetic Kidney Disease in a Mouse Model of Type 1 Diabetes

2015; Hindawi Publishing Corporation; Volume: 2015; Linguagem: Inglês

10.1155/2015/653260

1466-1861

Charlotte B. Holt, Jakob Appel Østergaard, Esben Axelgaard, Gitte Krogh Nielsen, Yuichi Endo, Steffen Thiel, Troels Krarup Hansen,

Apelin-related biomedical research

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.