Increased inflammation in older high-pressure glaucoma mice.

Area of Science:

• Ophthalmology
• Gerontology
• Immunology

Background:

• Glaucoma risk increases with age and elevated intraocular pressure (IOP).
• Understanding the interplay between aging and inflammation in glaucoma is crucial for therapeutic development.

Purpose of the Study:

• To investigate inflammatory and aging processes in high-pressure glaucoma mice compared to age-matched controls.
• To explore the association between inflammation, cellular senescence, and glaucoma progression.

Main Methods:

• Utilized 20-month-old βB1-Connective Tissue Growth Factor (βB1-CTGF) glaucoma mice and wildtype (WT) controls.
• Performed intraocular pressure (IOP) measurements, histological analyses, and quantitative real-time PCR.
• Assessed retinal ganglion cell counts, macrogliosis, microglia/macrophage presence, inflammatory cytokine levels, and senescence markers.

Main Results:

• βB1-CTGF mice exhibited significantly higher IOP and reduced retinal ganglion cell numbers compared to WT controls.
• Glaucoma mice showed increased macrogliosis, microglia/macrophage infiltration, and elevated levels of Interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and transforming growth factor-β2.
• Enhanced senescence-associated β-galactosidase staining and decreased Lmnb1 mRNA levels were observed in βB1-CTGF retinas.

Conclusions:

• High-pressure glaucoma in aged mice is associated with heightened inflammation and cellular aging processes.
• Findings suggest a significant link between inflammation and glaucoma pathogenesis.
• Results may inform the development of novel therapeutic strategies for glaucoma.