Glaucoma Research with EZ4U Cell Viability Assay
Glaucoma is one of the leading causes of blindness worldwide, characterized by the loss of retinal ganglion cells (RGCs). Since vision loss from glaucoma is irreversible, early therapeutic intervention is critically important. However, due to current limitations in assessing glaucomatous neurodegeneration, it remains challenging to objectively monitor disease severity and progression, hindering the development of targeted treatment strategies (1, 2).
Glaucoma Research with EZ4U Cell Viability Assay
Our EZ4U (easy for you) cell proliferation and cytotoxicity assay was highlighted in a recent study that explored the critical involvement of PEDF in zinc-related pathways contributing to neurodegeneration in glaucoma : A role of pigment epithelium-derived factor in zinc-mediated mechanism of neurodegeneration in glaucoma. Insights from this research could pave the way for novel therapeutic strategies
– Non-radioactive & non-toxic assay
– Reliable & sensitive
– Convenient single-step incubation-for use on living cells
– Widely cited in more than 294 citations
Glaucoma Research with EZ4U Cell Viability Assay
A role of pigment epithelium-derived factor in zinc-mediated mechanism of neurodegeneration in glaucoma. Chistyakov DV et al., Commun Biol. 2025 Jul 1;8(1):965. PMID: 40596696.
Abstract
Glaucoma is a neurodegenerative condition involving optic nerve damage and retinal ganglion cells death. Animal studies suggested that the pathway linking these events can be mediated by mobile zinc secreted into the intraretinal space and exerting cytotoxic effects. Whether this mechanism is relevant for human glaucoma and what are the targets of extracellular zinc is unknown. We report that increased zinc content in the aqueous humor and retina is indeed a characteristic of glaucomatous neuropathy, and excess extracellular zinc may be recognized by the key retinal neurotrophic factor PEDF. Biophysical and X-ray crystallographic studies show that PEDF coordinates zinc ions in five types of intermolecular high-affinity sites, leading to a decrease in negative surface charge and reversible oligomerization of the protein, thereby masking the target recognition sites responsible for its neurotrophic and antiangiogenic activities and collagen binding. Notably, PEDF secretion is enhanced in both glaucoma and retinal cell models in response to zinc stress; however, zinc binding negatively affects axogenic, differentiative and prosurvival functions of PEDF by suppressing its ability to activate receptor PEDF-R/PNPLA2. We suggest that glaucomatous neurodegeneration is associated with direct inhibition of PEDF signaling by extracellular zinc, making their complex a promising target for neuroprotective therapy.
Literature:
- Glaucoma: now and beyond. Lancet. Jayaram H, Kolko M, Friedman DS, Gazzard G. 2023 Nov 11;402(10414):1788-1801. doi: 10.1016/S0140-6736(23)01289-8. Epub 2023 Sep 21. PMID: 37742700.
- Glaucoma in Adults-Screening, Diagnosis, and Management: A Review. Stein JD, Khawaja AP, Weizer JS. JAMA. 2021 Jan 12;325(2):164-174. doi: 10.1001/jama.2020.21899. PMID: 33433580.
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