ArticleScientific reports2016
Dose- and time-dependent effects of actomyosin inhibition on live mouse outflow resistance and aqueous drainage tissues.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Aqueous humor TGFβ and fibrillin-1 in Tsk mice reveal clues to POAG pathogenesis.Scientific reports · 2024Article
- Measurement of postmortem outflow facility using iPerfusion.Experimental eye research · 2022Article
- Fibrillin-1 mutant mouse captures defining features of human primary open glaucoma including anomalous aqueous humor TGF beta-2.Scientific reports · 2022Article
- Aqueous Humor Dynamics of the Brown-Norway Rat.Investigative ophthalmology & visual science · 2018Article
- High-Resolution, Three-Dimensional Reconstruction of the Outflow Tract Demonstrates Segmental Differences in Cleared Eyes.Investigative ophthalmology & visual science · 2018Article
- Deep tissue analysis of distal aqueous drainage structures and contractile features.Scientific reports · 2017Article
- Toward in vivo two-photon analysis of mouse aqueous outflow structure and function.Experimental eye research · 2017Review
- Aqueous outflow regulation: Optical coherence tomography implicates pressure-dependent tissue motion.Experimental eye research · 2017Review
- Aqueous outflow - A continuum from trabecular meshwork to episcleral veins.Progress in retinal and eye research · 2017Review
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Actomyosin contractility modulates outflow resistance of the aqueous drainage tissues and intraocular pressure, a key pathogenic factor of glaucoma. We established methodology to reliably analyze the effect of latrunculin-B (Lat-B)-induced actin depolymerization on outflow physiology in live mice. A voltage-controlled microperfusion system for delivering drugs and simultaneously analyzing outflow resistance was tested in live C57BL/6 mice. Flow rate and perfusion pressure were reproducible within a coefficient of variation of 2%. Outflow facility for phosphate-buffered saline (0.0027 ± 0.00036 μL/min/mmHg; mean ± SD) and 0.02% ethanol perfusions (Lat-B vehicle; 0.0023 ± 0.0005 μL/min/mmHg) were similar and stable over 2 hours (p > 0.1 for change), indicating absence of a 'washout' artifact seen in larger mammals. Outflow resistance changed in graded fashion, decreasing dose- and time-dependently over 2 hours for Lat-B doses of 2.5 μM (p = 0.29), 5 μM (p = 0.039) and 10 μM (p = 0.001). Resulting outflow resistance was about 10 times lower with 10 μM Lat-B than vehicle control. The filamentous actin network was decreased and structurally altered in the ciliary muscle (46 ± 5.6%) and trabecular meshwork (37 ± 8.3%) of treated eyes relative to vehicle controls (p < 0.005; 5 μM Lat-B). Mouse actomyosin contractile mechanisms are important to modulating aqueous outflow resistance, mirroring mechanisms in primates. We describe approaches to reliably probe these mechanisms in vivo.
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