Ace Therapeutics specializes in developing genetic mouse models and offering comprehensive preclinical services for glaucoma research. Our expertise enables researchers to better understand the mechanisms of glaucoma and develop innovative therapeutic strategies
Slc1a3 in Glaucoma: Unveiling Pathogenic Mechanisms
The Slc1a3 gene encodes the solute carrier family 1 member 3 (SLC1A3) protein, also known as the glutamate–aspartate transporter. This transporter is predominantly expressed in retinal Müller glial cells. It clears extracellular glutamate to prevent excitotoxicity in retinal ganglion cells (RGCs) and facilitates cysteine uptake for glutathione synthesis, protecting RGCs from oxidative stress. Loss of Slc1a3 function leads to spontaneous RGC degeneration and optic nerve damage even without elevated intraocular pressure (IOP), making Slc1a3-deficient mouse models particularly valuable for studying normal tension glaucoma (NTG). The dual role of SLC1A3 in mediating excitotoxicity prevention and oxidative stress protection highlights it as a central target in glaucoma research.
Fig. 1 Glutamatergic synaptic transduction and uptake and metabolism of glutamate in the Müller cell. (Makoto I., 2013)
Explore Ace Therapeutics' Custom Slc1a3 Mutant Mouse Models
With years of experience in the development of preclinical ophthalmic models, Ace Therapeutics can provide custom Slc1a3 mutant mouse models that recapitulate key features of NTG.
| Model types | Model characteristics | Applications |
|---|---|---|
| Slc1a3-KO mice | Homozygous knockout with spontaneous RGC and optic nerve degeneration without elevated IOP. | Ideal for studying NTG pathogenesis. |
| Slc1a3-Flox mice | Conditional allele; phenotype depends on targeted deletion, allowing region- or cell-specific Slc1a3 loss. | Useful for dissecting cell-specific roles of Slc1a3 in retinal health and glaucoma. |
Our Slc1a3 Mutant Mouse Model Evaluation Services
Our comprehensive evaluation services enable detailed analysis of Slc1a3 mutant mouse models, empowering researchers to investigate glaucoma pathogenesis and evaluate potential therapeutics.
- Retinal histology and immunohistochemistry: Evaluate RGC degeneration, quantify RGC loss, and analyze glutamate transporter expression and localization.
- Optic nerve analysis: Assess optic nerve damage by histological analysis and axon counting.
- Retinal function assessment: Evaluate retinal function and visual responses by multifocal electroretinography (mfERG), and detect structural damage to the retina and optic nerve by optical coherence tomography (OCT).
- Biochemical assays: Measure key biochemical markers relevant to glaucoma pathogenesis, including glutamate and glutathione levels as well as oxidative stress markers.
Ace Therapeutics supports normal tension glaucoma research with custom Slc1a3 mutant mouse models that serve as invaluable tools for studying disease mechanisms and evaluating therapeutics. Ready to unlock new insights into normal tension glaucoma research? Contact us today to discuss how we can tailor these solutions to your needs!
Reference
- Makoto I. Abnormalities in Glutamate Metabolism and Excitotoxicity in the Retinal Diseases. Scientifica (Cairo), 2013, 2013: 528940.