ArticleInvestigative ophthalmology & visual science2011
Cytoskeletal dependence of adenosine triphosphate release by human trabecular meshwork cells.
Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Mechanistic Effects of Baicalein on Aqueous Humor Drainage and Intraocular Pressure.International journal of molecular sciences · 2022Article
- Recent advances in understanding the role of metabolic heterogeneities in cell migration.Faculty reviews · 2021Review
- Neuroinflammation in Primary Open-Angle Glaucoma.Journal of clinical medicine · 2020Review
- Aqueous Humor Outflow Requires Active Cellular Metabolism in Mice.Investigative ophthalmology & visual science · 2020Article
- The β4-Subunit of the Large-Conductance Potassium Ion Channel KCa1.1 Regulates Outflow Facility in Mice.Investigative ophthalmology & visual science · 2020Article
- Effect and Mechanism of Phosphodiesterase Inhibitors on Trabecular Outflow.Korean journal of ophthalmology : KJO · 2019Article
- Targeting Schlemm's Canal in the Medical Therapy of Glaucoma: Current and Future Considerations.Advances in therapy · 2017Review
- VEGF as a Paracrine Regulator of Conventional Outflow Facility.Investigative ophthalmology & visual science · 2017Article
- Deregulation of ocular nucleotide homeostasis in patients with diabetic retinopathy.Journal of molecular medicine (Berlin, Germany) · 2017Article
- Differential response and withdrawal profile of glucocorticoid-treated human trabecular meshwork cells.Experimental eye research · 2017Article
- Regulatory Roles of Anoctamin-6 in Human Trabecular Meshwork Cells.Investigative ophthalmology & visual science · 2017Article
- Ocular Purine Receptors as Drug Targets in the Eye.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2016Review
- Glucocorticoid therapy and ocular hypertension.European journal of pharmacology · 2016Review
- Temperature oscillations drive cycles in the activity of MMP-2,9 secreted by a human trabecular meshwork cell line.Investigative ophthalmology & visual science · 2015Article
- The role of activated adenosine receptors in degranulation of human LAD2 mast cells.Purinergic signalling · 2014Article
- Effects of cardiotonic steroids on trabecular meshwork cells: search for mediator of ouabain-enhanced outflow facility.Experimental eye research · 2012Article
- Current understanding of conventional outflow dysfunction in glaucoma.Current opinion in ophthalmology · 2012Review
- Mechanisms of ATP release, the enabling step in purinergic dynamics.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2011Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
purposeTo test whether adenosine triphosphate (ATP) release links cytoskeletal remodeling with release of matrix metalloproteinases (MMPs), regulators of outflow facility and intraocular pressure.
methodsATP release was measured by luciferin-luciferase. Ecto-ATPases from transformed human trabecular meshwork (TM) cells (TM5) and explant-derived TM cells were identified by RT-PCR. Actin was visualized by phalloidin staining. Cell viability was assayed by lactate dehydrogenase and thiazolyl blue tetrazolium bromide methods and propidium iodide exclusion, gene expression by real-time PCR, and MMP release by zymography. Cell volume was monitored by electronic cell sorting.
resultsHypotonicity (50%) and mechanical stretch increased ATP release with similar pharmacologic profiles. TM cells expressed ecto-ATPases E-NPP1-3, E-NTPD2, E-NTPD8, and CD73. Prolonged dexamethasone (DEX) exposure (≥ 2 weeks), but not brief exposure (3 days), increased cross-linked actin networks and reduced swelling-triggered ATP release. Cytochalasin D (CCD) exerted opposite effects. Neither DEX nor CCD altered the cell viability, gene expression, or pharmacologic profile of ATP-release pathways. DEX accelerated, and CCD slowed, the regulatory volume decrease after hypotonic exposure. Activating A(1) adenosine receptors (A(1)ARs) increased total MMP-2 and MMP-9 release. DEX reduced total A(1)AR-triggered MMP release, and CCD increased the active form of MMP-2 release. The A(1)AR agonist CHA and the A(1)AR antagonist DPCPX partially reversed the effects of DEX and CCD, respectively.
conclusionsCytoskeletal restructuring modulated swelling-activated ATP release, in part by changing the duration of cell swelling after hypotonic challenge. Modifying ATP release is expected to modulate MMP secretion by altering ecto-enzymatic delivery of adenosine to A(1)ARs, linking cytoskeletal remodeling and MMP-mediated modulation of outflow facility.
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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.