0000000000414079

AUTHOR

Karl Mercieca

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.…

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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…

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Canaloplasty with mitomycin C after previous combined cataract surgery and Schlemm's canal microstent implantation.

We report on a 56-year-old male with primary open-angle glaucoma who underwent mitomycin C augmented canaloplasty enabling filtration in the right eye after cataract surgery combined with a Schlemm’s canal microstent 3 years previously. He showed progressive glaucomatous optic neuropathy and was highly myopic (axial length 32.05 mm, spherical equivalent −18.75 dioptres in the right eye). Augmented canaloplasty was performed uneventfully and 360° catheterisation was achieved followed by the placement of a 10-0 polypropylene suture in Schlemm’s canal. Intraocular pressure (IOP) in the first post-operative day was reduced from 19 to 6 mmHg. At 1-month follow-up IOP was 12 mmHg off glaucoma me…

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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…

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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

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Anterior Corneal Folds in Postoperative Hypotony Following Glaucoma Drainage Surgery

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Management of Descemet's membrane haemorrhage after canaloplasty

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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.

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