@article{NeuhausBurekDjuzenovaetal.2012,
  author    = {Neuhaus, Winfried and Burek, Malgorzata and Djuzenova, Cholpon C and Thal, Serge C and Koepsell, Hermann and Roewer, Norbert and F{\"o}rster, Carola Y},
  title     = {Addition of NMDA-receptor antagonist MK801 during oxygen/glucose deprivation moderately attenuates the up-regulation of glucose uptake after subsequent reoxygenation in brain endothelial cells},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-67241},
  year      = {2012},
  abstract  = {During stroke the blood-brain barrier (BBB) is damaged which can result in vasogenic brain edema and inflammation. The reduced blood supply leads to decreased delivery of oxygen and glucose to affected areas of the brain. Oxygen and glucose deprivation (OGD) can cause upregulation of glucose uptake of brain endothelial cells. In this letter, we investigated the influence of MK801, a non-competitive inhibitor of the NMDA-receptor, on the regulation of the glucose uptake and of the main glucose transporters glut1 and sglt1 in murine BBB cell line cerebEND during OGD. mRNA expression of glut1 was upregulated 68.7- fold after 6 h OGD, which was significantly reduced by 10 μM MK801 to 28.9-fold. Sglt1 mRNA expression decreased during OGD which was further reduced by MK801. Glucose uptake was significantly increased up to 907\% after 6 h OGD and was still higher (210\%) after the 20 h reoxygenation phase compared to normoxia. Ten micromolar MK801 during OGD was able to reduce upregulated glucose uptake after OGD and reoxygenation significantly. Presence of several NMDAR subunits was proven on the mRNA level in cerebEND cells. Furthermore, it was shown that NMDAR subunit NR1 was upregulated during OGD and that this was inhibitable by MK801. In conclusion, the addition of MK801 during the OGD phase reduced significantly the glucose uptake after the subsequent reoxygenation phase in brain endothelial cells.},
  subject      = {Blut-Hirn-Schranke},
  language  = {en}
}
@article{KarnatiGuntasRajendranetal.2022,
  author    = {Karnati, Srikanth and Guntas, Gulcan and Rajendran, Ranjithkumar and Shityakov, Sergey and H{\"o}ring, Marcus and Liebisch, Gerhard and Kosanovic, Djuro and Erg{\"u}n, S{\"u}leyman and Nagai, Michiaki and F{\"o}rster, Carola Y.},
  title     = {Quantitative lipidomic analysis of Takotsubo syndrome patients' serum},
  series = {Frontiers in Cardiovascular Medicine},
  volume    = {9},
  journal   = {Frontiers in Cardiovascular Medicine},
  number    = {797154},
  issn      = {2297-055X},
  doi       = {10.3389/fcvm.2022.797154},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-270832},
  year      = {2022},
  abstract  = {Takotsubo syndrome (TTS), also known as the transient left ventricular apical ballooning syndrome, is in contemporary times known as novel acute cardiac syndrome. It is characterized by transient left ventricular apical akinesis and hyperkinesis of the basal left ventricular portions. Although the precise etiology of TTS is unknown, events like the sudden release of stress hormones, such as the catecholamines and the increased inflammatory status might be plausible causes leading to the cardiovascular pathologies. Recent studies have highlighted that an imbalance in lipid accumulation might promote a deviant immune response as observed in TTS. However, there is no information on comprehensive profiling of serum lipids of TTS patients. Therefore, we investigated a detailed quantitative lipid analysis of TTS patients using ES-MSI. Our results showed significant differences in the majority of lipid species composition in the TTS patients compared to the control group. Furthermore, the computational analyses presented was able to link the altered lipids to the pro-inflammatory cytokines and disseminate possible mechanistic pathways involving TNFα and IL-6. Taken together, our study provides an extensive quantitative lipidome of TTS patients, which may provide a valuable Pre-diagnostic tool. This would facilitate the elucidation of the underlying mechanisms of the disease and to prevent the development of TTS in the future.},
  language  = {en}
}
@article{ShityakovNagaiErguenetal.2022,
  author    = {Shityakov, Sergey and Nagai, Michiaki and Erg{\"u}n, S{\"u}leyman and Braunger, Barbara M. and F{\"o}rster, Carola Y.},
  title     = {The protective effects of neurotrophins and microRNA in diabetic retinopathy, nephropathy and heart failure via regulating endothelial function},
  series = {Biomolecules},
  volume    = {12},
  journal   = {Biomolecules},
  number    = {8},
  issn      = {2218-273X},
  doi       = {10.3390/biom12081113},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-285966},
  year      = {2022},
  abstract  = {Diabetes mellitus is a common disease affecting more than 537 million adults worldwide. The microvascular complications that occur during the course of the disease are widespread and affect a variety of organ systems in the body. Diabetic retinopathy is one of the most common long-term complications, which include, amongst others, endothelial dysfunction, and thus, alterations in the blood-retinal barrier (BRB). This particularly restrictive physiological barrier is important for maintaining the neuroretina as a privileged site in the body by controlling the inflow and outflow of fluid, nutrients, metabolic end products, ions, and proteins. In addition, people with diabetic retinopathy (DR) have been shown to be at increased risk for systemic vascular complications, including subclinical and clinical stroke, coronary heart disease, heart failure, and nephropathy. DR is, therefore, considered an independent predictor of heart failure. In the present review, the effects of diabetes on the retina, heart, and kidneys are described. In addition, a putative common microRNA signature in diabetic retinopathy, nephropathy, and heart failure is discussed, which may be used in the future as a biomarker to better monitor disease progression. Finally, the use of miRNA, targeted neurotrophin delivery, and nanoparticles as novel therapeutic strategies is highlighted.},
  language  = {en}
}
@article{ReschkeSalvadorSchlegeletal.2022,
  author    = {Reschke, Moritz and Salvador, Ellaine and Schlegel, Nicolas and Burek, Malgorzata and Karnati, Srikanth and Wunder, Christian and F{\"o}rster, Carola Y.},
  title     = {Isosteviol sodium (STVNA) reduces pro-inflammatory cytokine IL-6 and GM-CSF in an in vitro murine stroke model of the blood-brain barrier (BBB)},
  series = {Pharmaceutics},
  volume    = {14},
  journal   = {Pharmaceutics},
  number    = {9},
  issn      = {1999-4923},
  doi       = {10.3390/pharmaceutics14091753},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-286275},
  year      = {2022},
  abstract  = {Early treatment with glucocorticoids could help reduce both cytotoxic and vasogenic edema, leading to improved clinical outcome after stroke. In our previous study, isosteviol sodium (STVNA) demonstrated neuroprotective effects in an in vitro stroke model, which utilizes oxygen-glucose deprivation (OGD). Herein, we tested the hypothesis that STVNA can activate glucocorticoid receptor (GR) transcriptional activity in brain microvascular endothelial cells (BMECs) as previously published for T cells. STVNA exhibited no effects on transcriptional activation of the glucocorticoid receptor, contrary to previous reports in Jurkat cells. However, similar to dexamethasone, STVNA inhibited inflammatory marker IL-6 as well as granulocyte-macrophage colony-stimulating factor (GM-CSF) secretion. Based on these results, STVNA proves to be beneficial as a possible prevention and treatment modality for brain ischemia-reperfusion injury-induced blood-brain barrier (BBB) dysfunction.},
  language  = {en}
}