The University of Tokyo · Medicine
Professor Makoto Aihara's research lab focuses on the molecular and physiological mechanisms underlying intraocular pressure (IOP) regulation and glaucomatous optic neuropathy. The lab investigates the role of extracellular signaling molecules—particularly the autotaxin (ATX)-lysophosphatidic acid (LPA) pathway—in IOP homeostasis and glaucoma pathogenesis, using genetically engineered mouse models. They also explore the therapeutic potential of ocular drugs, such as prostaglandin analogues, in modulating IOP and adipogenesis in ocular tissues. The lab employs translational mouse models to study aqueous humor dynamics, collagen metabolism, and drug responses, aiming to uncover novel targets for glaucoma treatment.
Figures are computed from collected data and may differ slightly.
The mouse eye has similar aqueous production and aqueous humor turnover rate as the human eye. The presence of both conventional and uveoscleral outflow suggests that the mouse is a useful model system for further investigations of the biology of aqueous dynamics.
This method produces persistent IOP elevation in mouse eyes and may be a promising experimental model for the investigation of the biological mechanisms of glaucomatous optic neuropathy.
Latanoprost reduces mouse IOP in a dose-dependent manner. The mouse may be a useful model for studying the effect of drugs on IOP.
These results demonstrate ocular hypertension in mice with a targeted type I collagen mutation and suggest there is an association between IOP regulation and fibrillar collagen turnover.
Prostaglandin analogues have the potential to inhibit adipogenesis through FP receptor stimulation. Although these findings should be further analyzed in model systems more closely related to orbital fat, PG analogues may directly lead to reduced orbital fat by inhibiting adipogenesis.
Bioactive ATX/LPA/LPC concentrations were present in aqueous humor, and higher ATX and LPA concentrations were significantly correlated with IOP in all study subjects. Furthermore, the ATX-LPA pathway was significantly related to glaucoma subtype. These results reveal the potentially important role of the ATX-LPA pathway for IOP regulation in healthy subjects and glaucoma patients.
The carboxyfluorescein permeability assay using HCES in a serum-free system was the most useful for the quantification of toxicity of ophthalmic solutions. Among the regimens examined, a BAC concentration of 0.001% or lower or non-BAC preservative sofZia was suggested to be the least toxic to the ocular surface.
Mouse EVP was successfully measured based on the detection of erythrocyte reflux from an episcleral vein into Schlemm's canal. Both EVP and IOP increased with the degree of the head-down body position.
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