0000000000414082
AUTHOR
Hanhan Liu
Chronic social defeat stress causes retinal vascular dysfunction
Abstract Purpose The roles of vascular dysfunction and chronic stress have been extensively discussed in the pathophysiology of glaucoma. Our aim was to test whether chronic stress causes retinal vascular dysfunction and therewith induces retinal ganglion cells (RGCs) loss. Methods Twelve mice underwent chronic social defeat (CSD) stress, while 12 mice received control treatment only. Intraocular pressure (IOP) was measured with a rebound tonometer. Blood plasma corticosterone concentration and adrenal gland weight were used to assess stress levels. Brn-3a staining in retinas and PPD staining in optic nerve cross sections were conducted to assess the survival of RGCs and axons respectively.…
Proteome alterations in aqueous humour of primary open angle glaucoma patients.
Aim To unravel the primary open angle glaucoma (POAG) related proteomic changes in aqueous humour (AH). Methods Totally 35 patients listed for cataract surgery (controls: n=12, age: 67.4±13.6y) or trabeculectomy for POAG (n=23, age: 72.5±8.3y) were included. AH samples of those patients were obtained during cataract surgery or trabeculectomy. AH samples were subsequently pooled into the experimental groups under equal contribution in terms of protein amount of each individual patient. Protein samples were analyzed by a linear trap quadrupol Orbitrap Mass Spectrometry device with an upstream liquid chromatography system. The obtained raw data were analyzed using the Maxquant proteome softwar…
Elevated intraocular pressure induces neuron-specific β-III-tubulin expression in non-neuronal vascular cells.
Purpose Pathological alterations within optic nerve axons and progressive loss of the parental retinal ganglion cell (RGC) bodies are characteristics of glaucomatous neuropathy. Abnormally elevated intraocular pressure (IOP) is thought to be the major risk factor for most forms of glaucomatous changes, while lowering of the IOP is the mainstream of treatment. However, the pathophysiological mechanisms involved in neurodegenerative changes are poorly understood. It remains still a matter of debate whether elevated IOP harms the neurons directly or indirectly through alterations in the retinal vascularization. Methods We analysed morphological and molecular changes within the retina exposed t…
Proteomics Reveals the Potential Protective Mechanism of Hydrogen Sulfide on Retinal Ganglion Cells in an Ischemia/Reperfusion Injury Animal Model
Glaucoma is the leading cause of irreversible blindness and is characterized by progressive retinal ganglion cell (RGC) degeneration. Hydrogen sulfide (H2S) is a potent neurotransmitter and has been proven to protect RGCs against glaucomatous injury in vitro and in vivo. This study is to provide an overall insight of H2S&rsquo
Mitochondrial Markers in Aging and Primary Open-Angle Glaucoma
This review focuses on recent progress in understanding the role of mitochondrial markers in the context of mitochondrial dysfunction in glaucoma and discussing new therapeutic approaches to modulate mitochondrial function and potentially lead to improved outcomes in glaucoma.
Alterations in Tight- and Adherens-Junction Proteins Related to Glaucoma Mimicked in the Organotypically Cultivated Mouse Retina Under Elevated Pressure
Purpose To scrutinize alterations in cellular interactions and cell signaling in the glaucomatous retina, mouse retinal explants were exposed to elevated pressure. Methods Retinal explants were prepared from C57bl6 mice and cultivated in a pressure chamber under normotensive (atmospheric pressure + 0 mm Hg), moderately elevated (30 mm Hg), and highly elevated (60 mm Hg) pressure conditions. The expression levels of proteins involved in the formation of tight junctions (zonula occludens 1 [ZO-1], occludin, and claudin-5) and adherens junctions (VE-cadherin and β-catenin) and in cell-signaling cascades (Cdc42 and activated Cdc42 kinase 1 [ACK1]), as well as the expression levels of the growth…
Erhöhter Augeninnendruck für 7 Wochen induziert lokale Gefäßveränderungen im experimentellen Glaukommodell in vivo
Zusammenfassung Hintergrund Peripapilläre Blutungen sind diagnostisch wegweisend für das Vorliegen des Glaukoms. Dennoch ist die Rolle der Gefäße der Retina und des Sehnervs in der Pathogenese des Glaukoms weitestgehend ungeklärt. Ziel dieser Studie war es, im experimentellen Glaukommodell die lokalen Veränderungen dieser Gefäße auf erhöhten Druck in vivo zu untersuchen. Material und Methoden Das Glaukom wurde durch Veröden dreier episkleraler Venen des linken Auges von weiblichen Sprague-Dawley-Ratten induziert (n = 6). In vivo erfolgte eine Messung der Gefäßkaliber mittels peripapillärem Scan des SD-OCT (Heidelberg Engineering) als Baseline sowie 7 Wochen nach Augeninnendruckerhöhung. Die…