ArticleInvestigative ophthalmology & visual science2016
An In Vitro Perfusion System to Enhance Outflow Studies in Mouse Eyes.
Article in Investigative ophthalmology & visual science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Bioengineered 3D Human Trabecular Meshwork Models for Outflow Physiology and Glaucoma Research.Bioengineering (Basel, Switzerland) · 2026Review
- Endothelial cell-specific postnatal deletion of Nos3 preserves intraocular pressure homeostasis via macrophage recruitment and NOS2 upregulation.The Journal of clinical investigation · 2025Article
- FYN regulates aqueous humor outflow and IOP through the phosphorylation of VE-CADHERIN.Nature communications · 2025Article
- Molecular Mechanisms of Glaucoma Pathogenesis with Implications to Caveolin Adaptor Protein and Caveolin-Shp2 Axis.Aging and disease · 2024Review
- Pressure Clamping During Ocular Perfusions Drives Nitric Oxide-Mediated Washout.Investigative ophthalmology & visual science · 2023Article
- Caveolin-1 in vascular health and glaucoma: A critical vascular regulator and potential therapeutic target.Frontiers in medicine · 2023Review
- Caveolar and non-Caveolar Caveolin-1 in ocular homeostasis and disease.Progress in retinal and eye research · 2022Review
- Measurement of postmortem outflow facility using iPerfusion.Experimental eye research · 2022Article
- A Role of Caveolae in Trabecular Meshwork Mechanosensing and Contractile Tone.Frontiers in cell and developmental biology · 2022Article
- The vital role for nitric oxide in intraocular pressure homeostasis.Progress in retinal and eye research · 2021Review
- Membrane cholesterol regulates TRPV4 function, cytoskeletal expression, and the cellular response to tension.Journal of lipid research · 2021Article
- Physiologic Consequences of Caveolin-1 Ablation in Conventional Outflow Endothelia.Investigative ophthalmology & visual science · 2020Article
- Aqueous Humor Dynamics of the Brown-Norway Rat.Investigative ophthalmology & visual science · 2018Article
- Caveolin-1 Protects Retinal Ganglion Cells against Acute Ocular Hypertension Injury via Modulating Microglial Phenotypes and Distribution and Activating AKT pathway.Scientific reports · 2017Article
- Caveolin-1 and Caveolin-2 Can Be Antagonistic Partners in Inflammation and Beyond.Frontiers in immunology · 2017Review
- Caveolin-1 modulates intraocular pressure: implications for caveolae mechanoprotection in glaucoma.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
purposeThe molecular mechanisms controlling aqueous humor (AQH) outflow and IOP need much further definition. The mouse is a powerful system for characterizing the mechanistic basis of AQH outflow. To enhance outflow studies in mice, we developed a perfusion system that is based on human anterior chamber perfusion culture systems. Our mouse system permits previously impractical experiments.
methodsWe engineered a computer-controlled, pump-based perfusion system with a platform for mounting whole dissected mouse eyes (minus lens and iris, ∼45% of drainage tissue is perfused). We tested the system's ability to monitor outflow and tested the effects of the outflow-elevating drug, Y27632, a rho-associated protein kinase (ROCK) inhibitor. Finally, we tested the system's ability to detect genetically determined decreases in outflow by determining if deficiency of the candidate genes Nos3 and Cav1 alter outflow.
resultsUsing our system, the outflow facility (C) of C57BL/6J mouse eyes was found to range between 7.7 and 10.4 nl/minutes/mm Hg (corrected for whole eye). Our system readily detected a 74.4% Y27632-induced increase in C. The NOS3 inhibitor L-NG-nitroarginine methyl ester (L-NAME) and a Nos3 null mutation reduced C by 28.3% and 35.8%, respectively. Similarly, in Cav1 null eyes C was reduced by 47.8%.
conclusionsWe engineered a unique perfusion system that can accurately measure changes in C. We then used the system to show that NOS3 and CAV1 are key components of mechanism(s) controlling outflow.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.