Publications by authors named "Andreas Schlotterer"
Aims/hypothesis: The receptor for AGEs (RAGE) is linked to proinflammatory pathology in a range of tissues. The objective of this study was to assess the potential modulatory role of RAGE in diabetic retinopathy.
Methods: Diabetes was induced in wild-type (WT) and Rage (-/-) mice (also known as Ager (-/-) mice) using streptozotocin while non-diabetic control mice received saline.
Article Synopsis
- The study investigated how human insulin and its analogues can protect against lifespan reduction and neuronal damage in the nematode Caenorhabditis elegans under high glucose conditions, similar to those found in diabetes.
- Results showed that insulin treatments countered the adverse effects of high glucose, reducing reactive oxygen species (ROS) and advanced glycation end-products (AGEs), while enhancing the activity of protective enzymes like superoxide dismutase (SOD).
- The beneficial effects of insulin were linked to a specific signaling pathway involving the daf-2 insulin receptor and the daf-16/FOXO transcription factor, which helps regulate detoxifying processes in the cells.
Rats expressing a transgenic polycystic kidney disease (PKD) gene develop photoreceptor degeneration and subsequent vasoregression, as well as activation of retinal microglia and macroglia. To target the whole neuroglialvascular unit, neuro- and vasoprotective Erythropoietin (EPO) was intraperitoneally injected into four-week old male heterozygous PKD rats three times a week at a dose of 256 IU/kg body weight. For comparison EPO-like peptide, lacking unwanted side effects of EPO treatment, was given five times a week at a dose of 10 µg/kg body weight.
View Article and Find Full Text PDFDiabetes induces vasoregression, neurodegeneration and glial activation in the retina. Formation of advanced glycation endoproducts (AGEs) is increased in diabetes and contributes to the pathogenesis of diabetic retinopathy. CD74 is increased in activated microglia in a rat model developing both neurodegeneration and vasoregression.
View Article and Find Full Text PDFInterphase nuclear architecture is disrupted and rapidly reformed with each cell division cycle. Successive cell generations exhibit a "memory" of this nuclear architecture, as well as for gene expression. Furthermore, many features of nuclear and mitotic chromosome structure are recognizably species and tissue specific.
View Article and Find Full Text PDFDeletions in mitochondrial DNA (mtDNA) accumulate during aging. Expression of the Caenorhabditis elegans apurinic/apyrimidinic endonuclease 1 (APE1) ortholog exo-3, involved in DNA repair, is reduced by 45% (P < 0.05) during aging of C.
View Article and Find Full Text PDFObjective: Establishing Caenorhabditis elegans as a model for glucose toxicity-mediated life span reduction.
Research Design And Methods: C. elegans were maintained to achieve glucose concentrations resembling the hyperglycemic conditions in diabetic patients.
Article Synopsis
- Research shows that the production of reactive oxygen species (ROS) in mitochondria is a key factor in aging, using the organism Caenorhabditis elegans as a model.
- A newly identified mechanism involves the modification of mitochondrial proteins by methylglyoxal (MG), a byproduct of glycolysis, which increases with age when the enzyme glyoxalase-1, responsible for detoxifying MG, becomes less active.
- Enhancing the activity of glyoxalase-1 can reduce these harmful modifications and lower ROS production, leading to an extended lifespan in C. elegans, while reducing its activity has the opposite effect.
Investigating the interaction of human endometrium and trophoblast during implantation is difficult in vitro and impossible in vivo. This study was designed to analyze the effect of trophoblast on endometrial stromal cells during implantation by comprehensive gene profiling. An in vitro coculture system of endometrial stromal cells with first-trimester trophoblast explants was established.
View Article and Find Full Text PDFObjective: We studied the association between polymorphisms in the UCP genes and diabetes complications in patients with type 1 diabetes.
Research Design And Methods: We analyzed 227 patients with type 1 diabetes using PCR and subsequent cleavage by restriction endonucleases for the promoter variants A-3826G in the UCP1 gene, G-866A in the UCP2 gene, and C-55T in the UCP3 gene.
Results: No effect of the A-3826G polymorphism in the UCP1 gene on diabetes complications was found.