Corina Wilding
University of Mainz
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Publication
Featured researches published by Corina Wilding.
Progress in Retinal and Eye Research | 2013
Katharina Bell; Oliver W. Gramlich; Nadine von Thun und Hohenstein-Blaul; Sabine Beck; Sebastian Funke; Corina Wilding; Norbert Pfeiffer; Franz H. Grus
Glaucoma is a chronic neurodegenerative disease and one of the leading causes of blindness. Several risk factors have been described, e.g. an elevated intraocular pressure (IOP), oxidative stress or mitochondrial dysfunction. Additionally, alterations in serum antibody profiles of glaucoma patients, upregulation (e.g. anti-HSP60, anti-MBP) and downregulation (e.g. anti-14-3-3), have been described, but it still remains elusive if the autoantibodies seen in glaucoma are an epiphenomenon or causative. However, it is known that elicited autoimmunity causes retinal ganglion cell loss resulting in glaucomatous-like damage and according to the autoaggressive nature of some autoantibodies we found antibody deposits in human glaucomatous retinae in a pro-inflammatory environment. Furthermore, glaucomatous serum has the potential to influence neuroretinal cell regulatory processes. Importantly, we demonstrate that some autoantibodies hold neuroprotective potential for neuroretinal cells. The protective nature of autoantibodies and the molecular mechanisms underlying the very sensitive equilibrium between autoaggression and protection remain subject of future examinations and offer promising target sites for new therapeutic approaches. Additionally, the changes in antibody profiles could be used as highly sensitive and specific marker for diagnostics purposes. Early diagnosis and intervention in risk patients would offer the chance of early treatment and to slow down the progression of glaucoma and delay the resulting blindness.
Current Opinion in Pharmacology | 2013
Oliver W. Gramlich; Katharina Bell; Nadine von Thun und Hohenstein-Blaul; Corina Wilding; Sabine Beck; Norbert Pfeiffer; Franz H. Grus
There is growing evidence showing an autoimmune involvement in the pathogenesis of glaucoma, and that alterations in natural occurring autoantibody levels play a key role. The upregulation of autoantibodies can be associated with fatal conditions, but several studies demonstrate that natural autoantibodies entail also protective characteristics and influence the protein expression of neuroretinal cells. A disbalance of natural occurring autoantibodies may shift the physiological equilibrium of protective immunity leading to a predisposition for developing glaucoma. This article highlights recent advances in understanding of autoimmune mechanisms in the pathogenesis of glaucoma.
PLOS ONE | 2014
Corina Wilding; Katharina Bell; Sabine Beck; Sebastian Funke; Norbert Pfeiffer; Franz H. Grus
The family of synuclein proteins (α, β and γ) are related to neurodegenerative disease e.g. Parkinson disease and Morbus Alzheimer. Additionally, a connection between γ-synuclein and glaucoma, a neurodegenerative disease characterized by a progressive loss of retinal ganglion cells, which finally leads to blindness, exists. The reason for the development of glaucoma is still unknown. Recent studies evaluating the participation of immunological components, demonstrate complex changed antibody reactivities in glaucoma patients in comparison to healthy people, showing not only up-regulations (e.g. alpha-fodrin antibody) but also down-regulations (e.g. γ-synuclein antibody) of antibodies in glaucoma patients. Up-regulated antibodies could be auto-aggressive, but the role of down-regulated antibodies is still unclear. Previous studies show a significant influence of the serum and the antibodies of glaucoma patients on protein expression profiles of neuroretinal cells. The aim of this study was to investigate the effect of γ-synuclein antibody on the viability and reactive oxygen species levels of a neuroretinal cell line (RGC-5) as well as their interaction with cellular proteins. We found a protective effect of γ-synuclein antibody resulting in an increased viability (up to 15%) and decreased reactive oxygen species levels (up to −12%) of glutamate and oxidative stressed RGC-5. These can be traced back to anti-apoptotic altered protein expressions in the mitochondrial apoptosis pathway indicated by mass spectrometry and validated by microarray analysis such as active caspase 3, bcl-2 associated-x-protein, S100A4, voltage-dependent anion channel, extracellular-signal-regulated-kinase (down-regulated) and baculoviral IAP repeat-containing protein 6, phosphorylated extracellular-signal-regulated-kinase (up-regulated). These changed protein expression are triggered by the γ-synuclein antibody internalization of RGC-5 we could see in immunohistochemical stainings. These findings let us assume a novel physiological function of γ-synuclein antibodies and give insights in the role of autoantibodies in glaucoma. We hypothesize that the down-regulation of autoantibodies found in glaucoma patients lead to a loss of protective autoimmunity.
Journal of Pharmacological Sciences | 2015
Corina Wilding; Katharina Bell; Sebastian Funke; Sabine Beck; Norbert Pfeiffer; Franz H. Grus
The pathogenesis of glaucoma, a common neurodegenerative disease, involves an immunologic component. Changes in the natural autoantibody profile of glaucoma patients were detected, showing not only up-regulated but also down-regulated immunoreactivities. In recent studies we were able to demonstrate that the antibody changes have a large influence on protein profiles of neuroretinal cells. Furthermore we could demonstrate neuroprotective potential of one of the down-regulated antibodies (γ-synuclein antibody). Anti-GFAP antibody is another antibody found down-regulated in glaucoma patients. Since GFAP expression is intensified in glaucomatous retina, the aim of this study was to detect the effect of GFAP antibodies on neuroretinal cells. This is realized with a viability-test as well as proteomic analysis of cells incubated with GFAP antibodies. Furthermore, possible interaction partners of the GFAP antibody in neuroretinal cells were identified by western blot, mass spectrometry and indirect immunofluorescence staining. We found that the GFAP antibody is able to protect cells from oxidative stress, which is due to changed protein expressions of the actin cytoskeleton. Furthermore we detected a cross-reaction of the antibody to endoplasmic reticulum resident protein 57 on the cell membrane, which seems to lead to a changed signaling in the cells triggering the protective effects.
Journal of Neurochemistry | 2016
Katharina Bell; Corina Wilding; Sebastian Funke; Natarajan Perumal; Sabine Beck; Dominik Wolters; Jana Holz-Müller; Norbert Pfeiffer; Franz H. Grus
Glaucoma, a neurodegenerative disease, is characterized by a progressive loss of retinal ganglion cells (rgc). Up‐ and down‐regulated autoantibody immunoreactivities in glaucoma patients have been demonstrated. Previous studies showed protective effects of down‐regulated antibodies [gamma (γ)‐synuclein and glial fibrillary acidic protein [GFAP]) on neuroretinal cells. The aim of this study was to test these protective antibody effects on rgc in an organ culture model and to get a better understanding of cell–cell interactions of the retina in the context of the protective effect. We used an adolescent retinal organ culture (pig) with an incubation time of up to 4 days. Retinal explants were incubated with different antibodies for 24 h (anti‐GFAP, anti‐γ‐synuclein and anti‐myoglobin antibody as a control). Brn3a and TUNEL staining were performed. We also conducted glutamine synthetase staining and quantification of the retinal explants. Mass spectrometry analyses were performed as well as protein analyses via microarray. We detected a continuous decrease of rgc/mm in the retinal explants throughout the 4 days of incubation with increased TUNEL rgc staining. Immunohistochemical analyses showed a protective effect of anti‐γ‐synuclein (increased rgc/mm of 41%) and anti‐GFAP antibodies (increased rgc/mm of 37%). Mass spectrometric, microarray and immunohistochemical analyses demonstrated Müller cell involvement and decreased endoplasmic reticulum stress response in the antibody‐treated retinae. We could detect that the tested antibodies have a protective effect on rgc which seems to be the result of reduced stress levels in the retina as well as a shift of glutamine synthetase localization in the endfeet of the Müller cells towards the inner retinal layer.
BMC Ophthalmology | 2015
Katharina Bell; Corina Wilding; Sebastian Funke; Norbert Pfeiffer; Franz H. Grus
Investigative Ophthalmology & Visual Science | 2012
Katharina Bell; Corina Wilding; Norbert Pfeiffer; Franz H. Grus
Investigative Ophthalmology & Visual Science | 2017
Katharina Bell; Corina Wilding; Sabine Beck; Norbert Pfeiffer; Franz H. Grus
Investigative Ophthalmology & Visual Science | 2016
Katharina Bell; Corina Wilding; Jana Holz-Müller; Sebastian Funke; Norbert Pfeiffer; Franz H. Grus
Investigative Ophthalmology & Visual Science | 2015
Katharina Bell; Corina Wilding; Natarajan Perumal; Norbert Pfeiffer; Franz H. Grus