ArticleAmerican journal of physiology. Cell physiology2011
S1P₂ receptor regulation of sphingosine-1-phosphate effects on conventional outflow physiology.
Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- The Specific ROCK2 Inhibitor KD025 Alleviates Glycolysis through Modulating STAT3-, CSTA- and S1PR3-Linked Signaling in Human Trabecular Meshwork Cells.Biomedicines · 2024Article
- Pressure Clamping During Ocular Perfusions Drives Nitric Oxide-Mediated Washout.Investigative ophthalmology & visual science · 2023Article
- The RNA-binding protein and stress granule component ATAXIN-2 is expressed in mouse and human tissues associated with glaucoma pathogenesis.The Journal of comparative neurology · 2022Article
- Multiomics analysis reveals the mechanical stress-dependent changes in trabecular meshwork cytoskeletal-extracellular matrix interactions.Frontiers in cell and developmental biology · 2022Article
- TRPV4-Rho signaling drives cytoskeletal and focal adhesion remodeling in trabecular meshwork cells.American journal of physiology. Cell physiology · 2021Article
- Inflammatory Ocular Diseases and Sphingolipid Signaling.Advances in experimental medicine and biology · 2019Review
- Characterizing Sphingosine Kinases and Sphingosine 1-Phosphate Receptors in the Mammalian Eye and Retina.International journal of molecular sciences · 2018Article
- Gene transfer to the outflow tract.Experimental eye research · 2017Review
- Regulation of intraocular pressure by microRNA cluster miR-143/145.Scientific reports · 2017Article
- The Soluble Guanylate Cyclase Stimulator IWP-953 Increases Conventional Outflow Facility in Mouse Eyes.Investigative ophthalmology & visual science · 2016Article
- Physical Factors Affecting Outflow Facility Measurements in Mice.Investigative ophthalmology & visual science · 2015Article
- Role of nitric oxide in murine conventional outflow physiology.American journal of physiology. Cell physiology · 2015Article
- The formation of cortical actin arrays in human trabecular meshwork cells in response to cytoskeletal disruption.Experimental cell research · 2014Article
- Sphingolipids and ceramides of mouse aqueous humor: Comparative profiles from normotensive and hypertensive DBA/2J mice.Biochimie · 2014Article
- Sphingosine 1-phosphate receptors are essential mediators of eyelid closure during embryonic development.The Journal of biological chemistry · 2013Article
- What do mechanotransduction, Hippo, Wnt, and TGFβ have in common? YAP and TAZ as key orchestrating molecules in ocular health and disease.Experimental eye research · 2013Review
- Pharmacologic manipulation of conventional outflow facility in ex vivo mouse eyes.Investigative ophthalmology & visual science · 2012Article
- Protein markers and differentiation in culture for Schlemm's canal endothelial cells.Experimental eye research · 2012Article
- Current understanding of conventional outflow dysfunction in glaucoma.Current opinion in ophthalmology · 2012Review
- eNOS, a pressure-dependent regulator of intraocular pressure.Investigative ophthalmology & visual science · 2011Article
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevated intraocular pressure is the main risk factor in primary open-angle glaucoma, involving an increased resistance to aqueous humor outflow in the juxtacanalicular region of the conventional outflow pathway which includes the trabecular meshwork (TM) and the inner wall of Schlemm's canal (SC). Previously, sphingosine-1-phosphate (S1P) was shown to decrease outflow facility in porcine and human eyes, thus increasing outflow resistance and intraocular pressure. Owing to S1P's known effect of increasing barrier function in endothelial cells and the robust expression of the S1P₁ receptor on the inner wall of SC, we hypothesized that S1P₁ receptor activation promotes junction formation and decreases outflow facility. The effects of subtype-specific S1P receptor compounds were tested in human and porcine whole-eye perfusions and human primary cultures of SC and TM cells to determine the receptor responsible for S1P effects on outflow resistance. The S1P₁-specific agonist SEW2871 failed to both mimic S1P effects in paired human eye perfusions, as well as increase myosin light chain (MLC) phosphorylation in cell culture, a prominent outcome in S1P-treated SC and TM cells. In contrast, the S1P₂ antagonist JTE-013, but not the S1P₁ or S1P₁,₃ antagonists, blocked the S1P-promoted increase in MLC phosphorylation. Moreover, JTE-013 prevented S1P-induced decrease in outflow facility in perfused human eyes (P < 0.05, n = 6 pairs). Similarly, porcine eyes perfused with JTE-013 + S1P did not differ from eyes with JTE-013 alone (P = 0.53, n = 3). These results demonstrate that S1P₂ , and not S1P₁ or S1P₃, receptor activation increases conventional outflow resistance and is a potential target to regulate intraocular pressure.
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