Endogenous Regulation of Human Schlemm's Canal Cell Volume by Nitric Oxide Signaling

2010 ◽  
Vol 51 (11) ◽  
pp. 5817 ◽  
Author(s):  
Dorette Z. Ellis ◽  
Najam A. Sharif ◽  
William M. Dismuke
Keyword(s):  
Nitric Oxide ◽  
Cell Volume ◽  
Schlemm’S Canal ◽  
Nitric Oxide Signaling ◽  
Schlemm's Canal ◽  
Canal Cell ◽  
Endogenous Regulation

scholarly journals Role of nitric oxide in murine conventional outflow physiology

2015 ◽  
Vol 309 (4) ◽  
pp. C205-C214 ◽  
Author(s):  
Jason Y. H. Chang ◽  
W. Daniel Stamer ◽  
Jacques Bertrand ◽  
A. Thomas Read ◽  
Catherine M. Marando ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Fluorescent Protein ◽  
Detectable Effect ◽  
No Production ◽  
Schlemm’S Canal ◽  
Physiological Regulation ◽  
Outflow Facility ◽  
Aqueous Humor Outflow ◽  
Schlemm's Canal

Elevated intraocular pressure (IOP) is the main risk factor for glaucoma. Exogenous nitric oxide (NO) decreases IOP by increasing outflow facility, but whether endogenous NO production contributes to the physiological regulation of outflow facility is unclear. Outflow facility was measured by pressure-controlled perfusion in ex vivo eyes from C57BL/6 wild-type (WT) or transgenic mice expressing human endothelial NO synthase (eNOS) fused to green fluorescent protein (GFP) superimposed on the endogenously expressed murine eNOS (eNOS-GFPtg). In WT mice, exogenous NO delivered by 100 μM S-nitroso- N-acetylpenicillamine (SNAP) increased outflow facility by 62 ± 28% (SD) relative to control eyes perfused with the inactive SNAP analog N-acetyl-d-penicillamine (NAP; n = 5, P = 0.016). In contrast, in eyes from eNOS-GFPtg mice, SNAP had no effect on outflow facility relative to NAP (−9 ± 4%, P = 0.40). In WT mice, the nonselective NOS inhibitor NG-nitro-l-arginine methyl ester (l-NAME, 10 μM) decreased outflow facility by 36 ± 13% ( n = 5 each, P = 0.012), but 100 μM l-NAME had no detectable effect on outflow facility (−16 ± 5%, P = 0.22). An eNOS-selective inhibitor (cavtratin, 50 μM) decreased outflow facility by 19 ± 12% in WT ( P = 0.011) and 39 ± 25% in eNOS-GFPtg ( P = 0.014) mice. In the conventional outflow pathway of eNOS-GFPtg mice, eNOS-GFP expression was localized to endothelial cells lining Schlemm's canal and the downstream vessels, with no apparent expression in the trabecular meshwork. These results suggest that endogenous NO production by eNOS within endothelial cells of Schlemm's canal or downstream vessels contributes to the physiological regulation of aqueous humor outflow facility in mice, representing a viable strategy to more successfully lower IOP in glaucoma.

Effect of hydrostatic pressure gradients and Na2EDTA on permeability of human Schlemm's canal cell monolayers

2004 ◽  
Vol 28 (6) ◽  
pp. 391-398 ◽  
Author(s):  
A.G. Burke ◽  
W. Zhou ◽  
E.T. O'Brien ◽  
B.C. Roberts ◽  
W.D. Stamer
Keyword(s):  
Hydrostatic Pressure ◽  
Pressure Gradients ◽  
Schlemm’S Canal ◽  
Cell Monolayers ◽  
Schlemm's Canal ◽  
Canal Cell ◽  
Effect Of Hydrostatic Pressure

scholarly journals A Closer Look at Schlemm’s Canal Cell Physiology: Implications for Biomimetics

2015 ◽  
Vol 6 (3) ◽  
pp. 963-985 ◽  
Author(s):  
Cula Dautriche ◽  
Yangzi Tian ◽  
Yubing Xie ◽  
Susan Sharfstein
Keyword(s):  
Cell Physiology ◽  
Schlemm’S Canal ◽  
Schlemm's Canal ◽  
Canal Cell

scholarly journals Shear Stress-Triggered Nitric Oxide Release From Schlemm's Canal Cells

2014 ◽  
Vol 55 (12) ◽  
pp. 8067-8076 ◽  
Author(s):  
N. E. Ashpole ◽  
D. R. Overby ◽  
C. R. Ethier ◽  
W. D. Stamer
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Schlemm’S Canal ◽  
Nitric Oxide Release ◽  
Schlemm's Canal
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