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Meox2 Haploinsufficiency Accelerates Axonal Degeneration in DBA/2J Glaucoma
Rebecca A Buchanan1, Kate E Foley1,2, Keating W Pepper1
1The Jackson Laboratory, Bar Harbor, Maine, United States.
Investigative Ophthalmology & Visual Science
|August 2, 2019
Summary
Mesenchyme homeobox 2 (Meox2) loss in aging mice with glaucoma models increases axon damage. Meox2 regulates vascular remodeling and neuroinflammation, suggesting a therapeutic target for glaucoma prevention.
Area of Science:
- Ophthalmology
- Neuroscience
- Genetics
Background:
- Glaucoma is a complex optic neuropathy associated with aging and elevated intraocular pressure (IOP).
- Understanding early molecular events in glaucoma pathogenesis is crucial for developing novel therapeutics.
- DBA/2J mice serve as a relevant model for studying glaucoma-related changes.
Purpose of the Study:
- To identify and validate regulators of early gene expression changes in the DBA/2J mouse model of glaucoma.
- To investigate the role of mesenchyme homeobox 2 (Meox2) in the early stages of glaucoma.
Main Methods:
- Upstream regulator analysis (URA) was employed to identify potential master regulators of differentially expressed genes.
- Mesenchyme homeobox 2 (Meox2) function was assessed using genetic, biochemical, and immunofluorescence techniques.
- DBA/2J mice with Meox2 haploinsufficiency were analyzed for ocular phenotypes and gene expression.
Main Results:
- URA identified Meox2 as a key regulator in the optic nerve head of DBA/2J mice.
- Meox2 haploinsufficiency did not alter iris disease or IOP but significantly increased axon damage.
- Aged Meox2-deficient mice exhibited reduced MEOX2 protein levels, correlating with vascular and myeloid alterations.
Conclusions:
- Meox2 plays a critical role in controlling IOP-dependent vascular remodeling and neuroinflammation, thereby promoting axon survival.
- Targeting Meox2-mediated pathways before IOP elevation may offer a neuroprotective strategy for preventing human glaucoma.
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