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Cell-matrix's Response to Mechanical Forces01:13

Cell-matrix's Response to Mechanical Forces

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Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
09:03

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye

Published on: June 20, 2015

Cyclic mechanical stress and trabecular meshwork cell contractility.

Renata F Ramos1, Grant M Sumida, W Daniel Stamer

  • 1Biomedical Engineering Graduate Program, University of Arizona, Tucson, AZ 85711, USA.

Investigative Ophthalmology & Visual Science
|April 3, 2009
PubMed
Summary
This summary is machine-generated.

Ocular pulse increases intraocular pressure by affecting trabecular meshwork cells. This response, mediated by Rho-kinase, is blocked by Y27632, suggesting its role in outflow facility changes.

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Area of Science:

  • Ophthalmology
  • Cell Biology
  • Biophysics

Background:

  • Ocular pulse, a cyclic fluctuation in intraocular pressure (IOP), is known to decrease aqueous humor outflow facility.
  • The precise cellular mechanisms by which conventional outflow tissues, particularly the trabecular meshwork (TM), respond to these IOP oscillations remain largely uncharacterized.

Purpose of the Study:

  • To investigate the biomechanical responses of human trabecular meshwork (TM) cells to cyclic stress.
  • To determine the involvement of cell contractility in mediating these responses, using compounds that modulate it.

Main Methods:

  • Human TM cell monolayers were subjected to cyclic mechanical stress simulating ocular pulse (1-Hz frequency, 2.7 mm Hg amplitude).
  • Changes in intrachamber pressure and hydraulic conductivity were measured.
  • Immunocytochemistry and Western blot analysis assessed filamentous actin, stress fibers, and phosphorylated myosin light chain (p-MLC) levels.
  • Experiments were conducted with and without contractility-modulating agents (isoproterenol, Y27632, pilocarpine, nifedipine).

Main Results:

  • Cyclic stress significantly increased mean intrachamber pressure in TM cells, indicating decreased hydraulic conductivity (126.13% increase).
  • This pressure increase was abolished by Y27632, a Rho-kinase inhibitor, but not by other tested agents.
  • Y27632 also reduced p-MLC, filamentous/globular actin ratio, and stress fiber formation in TM cells.

Conclusions:

  • Human TM cells exhibit increased intrachamber pressure in response to cyclic mechanical stress.
  • The Rho-kinase signaling pathway and subsequent cellular contractility are critically involved in mediating the effects of ocular pulse on TM outflow facility.