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Custom Foxc2 Mutant Mouse Models of Glaucoma

Custom Foxc2 Mutant Mouse Models of Glaucoma

At Ace Therapeutics, we are dedicated to providing preclinical research services to accelerate the advancement of ocular therapy development. By leveraging our expertise in gene editing and ocular disease modeling, we offer custom Foxc2 mutant mouse models of glaucoma, enabling researchers to gain deep insights into glaucoma pathogenesis and evaluate the efficacy of therapeutic strategies.

FOXC2 is a Key Player in Glaucoma

Glaucoma, a leading cause of irreversible blindness globally, is often characterized by elevated intraocular pressure (IOP) resulting from compromised aqueous humor outflow. This outflow is primarily regulated by the trabecular meshwork (TM) and Schlemm's canal (SC) within the ocular anterior segment. FOXC2, a member of the forkhead box family of transcription factors, plays a critical role in the development and maintenance of ocular drainage structures such as the TM and SC. FOXC2 mutations or deficiencies can lead to abnormalities in the anterior segment structures, such as underdeveloped or absent SC and TM, which in turn disrupt aqueous humor outflow and elevate IOP.

Fig. 1 Corneal neovascularization and reduced SC area and volume in NC-Foxc2-/- mice as identified by Vis-OCTA and vis-OCT. Fig. 1 Vis-OCTA and vis-OCT identify corneal neovascularization and reduced SC area and volume in NC-Foxc2-/- mice. (Ujiie N, et al., 2023)

Custom Foxc2 Mutant Mouse Models of Glaucoma

Using genetic engineering techniques, our team of experts can develop tailored Foxc2 mutant mouse models that recapitulate human glaucoma-associated genetic conditions to support the investigation of cell type-specific FOXC2 functions in glaucoma pathogenesis.

Foxc2 Knockout Mouse Models of Glaucoma

  • Foxc2 haploinsufficient mice (Foxc2+/- mice)
    We offer custom generation of mice with a reduced copy number of the Foxc2 gene. These Foxc2+/- mice serve as essential tools for investigating the systemic effects of decreased FOXC2 level on overall ocular development and IOP regulation, reflecting conditions of haploinsufficiency observed in certain human glaucomatous diseases.
  • Cell-specific conditional knockout mice
    Our expert team is dedicated to developing genetically engineered mouse models with cell-specific conditional knockout of Foxc2 to support glaucoma research. For instance, we can develop neural crest (NC)-specific Foxc2 knockout mice to investigate the non-cell-autonomous role of FOXC2 in TM cells and its effects on SC development and IOP.

Foxc2 Knock-in Mouse Models of Glaucoma

We can provide Foxc2 knock-in mouse models in which the Foxc2 gene is inserted into the genome under the control of specific promoters to overexpress FOXC2 in target tissues.

Foxc2 Mutant Mouse Model Evaluation Services

In addition to our model generation capabilities, Ace Therapeutics offers a full range of preclinical research services designed to leverage Foxc2 mutant mouse models for studying glaucoma pathogenesis and supporting therapeutic development.

Services Details
IOP measurement
  • Measure IOP to determine whether Foxc2 deficiency leads to elevated IOP and clarify the relationship between anterior segment structural abnormalities and IOP changes.
Anterior segment morphological assessment
  • Use slit-lamp biomicroscopy and ophthalmoscopy to evaluate anterior chamber abnormalities, iris-corneal adhesions, corneal transparency, and pupil shape/position
  • Employ histology and immunohistochemistry to evaluate the cellular and tissue morphology of the TM, SC, iris, and ciliary body, and to identify the expression and localization of relevant proteins.
Glaucomatous neuropathy assessment
  • Assess the impact of anterior segment defects and elevated IOP on the posterior segment by evaluating retinal nerve fiber layer thickness.

Ace Therapeutics is your trusted partner in providing custom Foxc2 mutant mouse models for glaucoma research. Our comprehensive preclinical services are specifically designed to empower researchers to elucidate the underlying mechanisms of glaucoma and develop novel therapeutics. For more information about our services, please contact us directly.

References

  1. Smith R S, et al. Haploinsufficiency of the transcription factors Foxc1 and FOXC2 results in aberrant ocular development. Hum Mol Genet, 2000, 9(7): 1021-1032.
  2. Ujiie N, et al. Differential roles of FOXC2 in the trabecular meshwork and Schlemm's canal in glaucomatous pathology. Life Sci Alliance, 2023, 6(9): e202201721.

All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.

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