At Ace Therapeutics, we are dedicated to supporting glaucoma research by providing custom animal models. Our expertise lies in developing Prss56 mutant mouse models of glaucoma that allow researchers to explore the molecular mechanisms underlying angle-closure glaucoma (ACG) and identify novel therapeutic targets.
The Role of Prss56 in Glaucoma
Elevated intraocular pressure (IOP), a major risk factor for glaucoma, is mainly caused by inefficient aqueous humor outflow due to structural or functional changes in ocular drainage tissues such as the trabecular meshwork (TM) and Schlemm's canal. Prss56, encoding a serine protease, is vital for the development and maintenance of ocular drainage tissues and IOP homeostasis. Mutations in Prss56 impair the normal positioning of these tissues, leading to physical obstruction of the iridocorneal angle and subsequent elevation of IOP, making Prss56 an essential target for understanding ACG.
Fig. 1 Prss56 knockout mice show altered positioning of ocular angle structures. (Labelle-Dumais C, et al., 2020)
Explore Our Prss56 Mutant Mouse Models of Glaucoma
Ace Therapeutics provides a complete suite of services, from model development to in-depth phenotyping, saving you time and resources. Our team of experts provides comprehensive support throughout your research project.
Prss56 Null Mutant Mouse Models
With experience in generating and characterizing mouse models of glaucoma, our team of experts can construct Prss56 null mutant mice, which exhibit reduced ocular axial length and altered iridocorneal angle configuration, recapitulating key features of human ACG. Our Prss56 null mutant mouse models can be used to study the role of Prss56 loss-of-function in glaucoma pathogenesis and to develop therapeutic strategies.
Conditional Prss56 Mutant Mouse Models
We also offer conditional Prss56 mutant mouse models, allowing for tissue-specific or temporally controlled gene ablation. By utilizing gene editing technology, the expression of Prss56 can be selectively manipulated in the retina or other ocular tissues, providing insights into the spatiotemporal requirements of PRSS56 in ocular development and glaucoma.
Prss56 Mutant Mouse Model Evaluation Services
We provide a comprehensive suite of evaluation services to characterize the ocular phenotype of Prss56 mutant mouse models.
| Services | Details |
|---|---|
| IOP measurement | Longitudinal assessment of IOP using tonometry to monitor the development and progression of ocular hypertension. |
| Histological and morphometric analysis | Detailed examination of ocular tissues using immunohistochemistry and morphometry to assess structural alterations in the iridocorneal angle, retina, and optic nerve. |
| Optical coherence tomography (OCT) | In vivo imaging of ocular structures to visualize the iridocorneal angle and assess angle closure. |
| Aqueous humor outflow assessment | Measurement of aqueous humor outflow to determine the functional consequences of Prss56 mutations on fluid dynamics within the eye. |
| Retinal ganglion cell (RGC) quantification | Evaluation of RGC death by using techniques such as immunohistochemistry or retrograde labeling. |
As a preclinical contract research service provider, Ace Therapeutics is committed to supporting glaucoma basic research and drug development by providing custom Prss56 mutant mouse models. Our comprehensive services and scientific expertise make us the ideal partner for your research endeavors. Interested in our Prss56 mutant mouse models and specialized evaluation services? Contact us today to discover how we can support your research!
Reference
- Labelle-Dumais C, et al. Loss of PRSS56 function leads to ocular angle defects and increased susceptibility to high intraocular pressure. Dis Model Mech, 2020, 13(5): dmm042853.