ArticleInvestigative ophthalmology & visual science2009
Extracellular release of ATP mediated by cyclic mechanical stress leads to mobilization of AA in trabecular meshwork cells.
Article in Investigative ophthalmology & visual science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 47 citations in OpenAlex.
- Rodent Models of Glaucoma: How Mice and Rats Can Help Human Vision Move Out of the Woods and Into the Light.Cells · 2025Review
- Biomechanical properties of the trabecular meshwork in intraocular pressure regulation: a review.International ophthalmology · 2025Review
- TRPV4-Rho signaling drives cytoskeletal and focal adhesion remodeling in trabecular meshwork cells.American journal of physiology. Cell physiology · 2021Article
- Mechanical stretch induces CaScientific reports · 2021Article
- Reduced Pulsatile Trabecular Meshwork Motion in Eyes With Primary Open Angle Glaucoma Using Phase-Sensitive Optical Coherence Tomography.Investigative ophthalmology & visual science · 2020Article
- Article
- The β4-Subunit of the Large-Conductance Potassium Ion Channel KCa1.1 Regulates Outflow Facility in Mice.Investigative ophthalmology & visual science · 2020Article
- Mechanically induced autophagy is associated with ATP metabolism and cellular viability in osteocytes in vitro.Redox biology · 2018Article
- Article
- Cell culture: complications due to mechanical release of ATP and activation of purinoceptors.Cell and tissue research · 2017Review
- Hyperosmotic stress induces ATP release and changes in P2X7 receptor levels in human corneal and conjunctival epithelial cells.Purinergic signalling · 2017Article
- Autophagy and mechanotransduction in outflow pathway cells.Experimental eye research · 2017Review
- Aqueous outflow regulation: Optical coherence tomography implicates pressure-dependent tissue motion.Experimental eye research · 2017Review
- FOXC1 modulates MYOC secretion through regulation of the exocytic proteins RAB3GAP1, RAB3GAP2 and SNAP25.PloS one · 2017Article
- TRPV4 regulates calcium homeostasis, cytoskeletal remodeling, conventional outflow and intraocular pressure in the mammalian eye.Scientific reports · 2016Article
- OCT Study of Mechanical Properties Associated with Trabecular Meshwork and Collector Channel Motion in Human Eyes.PloS one · 2016Article
- Evidence for Extracellular ATP as a Stress Signal in a Single-Celled Organism.Eukaryotic cell · 2015Article
- MTOR-independent induction of autophagy in trabecular meshwork cells subjected to biaxial stretch.Biochimica et biophysica acta · 2014Article
- Evidence for Ca(2+)-regulated ATP release in gastrointestinal stromal tumors.Experimental cell research · 2013Article
- Optimizing gene transfer to conventional outflow cells in living mouse eyes.Experimental eye research · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
purposeTo investigate the mechanisms that mediate the release of ATP induced by cyclic mechanical stress (CMS) and the role of extracellular ATP in the mobilization of arachidonic acid (AA) and prostaglandin secretion.
methodsPorcine trabecular meshwork (pTM) cells were subjected to CMS. Extracellular ATP was detected with a luciferin-luciferase assay in the presence or absence of transport inhibitors and a lipid raft disrupter. ATP vesicles were visualized with quinacrine. The release of AA (AA 1-14C) was measured with and without ATP, ATP inhibitors, and phospholipase-A and -C inhibitors. Prostaglandin E2 (PGE2) and viability were measured with ELISA and a lactate dehydrogenase assay, respectively.
resultsCMS induced ATP release that was inhibited by the vesicle inhibitors N-ethylmaleimide (NEM) and monensin. Lipid raft disruption significantly increased the extracellular ATP induced by CMS. CMS induced AA release (1-4-fold increase) and its metabolic product PGE2 (3.9-fold increase). The AA mobilization induced by CMS could be mimicked by the addition of extracellular ATP and was partially inhibited by a P2 antagonist, by an ATP inhibitor, and by inhibitors of phospholipase-A2 and -C. Addition of PGE2 (10 microM) to the media exerted cytoprotective effects against long-term CMS.
conclusionsExtracellular release of ATP induced by CMS in TM cells is mediated by exocytosis of ATP-enriched vesicles into lipid rafts. The resulting activation of purinergic receptors leads to mobilization of AA from the plasma membrane. The subsequent release of PGE could exert protective effects by preventing TM cell loss that may result from chronic exposure to CMS.
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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.