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R. F. Ramos, W. D. Stamer; Cyclic Mechanical Stress and Trabecular Meshwork Cell Contractility. Invest. Ophthalmol. Vis. Sci. 2008;49(13):679.
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In the presence of ocular pulse (2.7 mmHg/sec), outflow facility of perfused anterior segments decreases. The exact mechanism by which conventional outflow tissues respond to cyclic pressure oscillations is unknown. The aim of the present study was to test the hypothesis that trabecular meshwork (TM) cell contractility mediates outflow facility responses to cyclic mechanical stress.
We modified an Ussing chamber perfusion system to deliver cyclic pressure oscillations while monitoring intrachamber pressure in real time (an inverse indicator of contraction-mediated changes in hydraulic conductivity). Mature human TM cell monolayers on polycarbonate filters were perfused at a constant flow rate of 2.5 µl/min until reaching a stable baseline pressure (5-20 mmHg). Chamber contents were exchanged using DMEM (control) or compounds known to affect cell contractility (isoproterenol, Y27632, pilocarpine and nifedipine). After reaching a new baseline, monolayers were subjected to cyclic stress averaging 2.7 mmHg at 1Hz for 2 hours; followed by 2 hours with no pressure oscillations.
Human TM monolayers respond to cyclic stress by increasing pressure during the pulsation period by 121.30±9.6% (n=8, p=0.002). In the presence of pilocarpine, TM cell response to cyclic stress was not different from pulse alone (129.54±34.6%; n=5, p=0.529). In contrast, isoproterenol caused an enhanced response to cyclic pressure oscillations (178.46±44.7%; n=5, p=0.006). The observed response to cyclic stress was blocked in the presence of Y27632 (98.62±16.2%; n=3, p=0.017).
Human TM cell monolayers respond to cyclic mechanical stress by decreasing hydraulic conductivity. Such a response can be enhanced or blocked by compounds known to alter cell contractility, suggesting a role for actino-myosin homeostasis in ocular pulse-mediated changes in outflow facility.
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