The role of the actomyosin system in regulating trabecular fluid outflow.
Abnormally high resistance to aqueous humor drainage via the trabecular meshwork and Schlemm's canal is highly correlated with the development of primary open-angle glaucoma. Contractility of the actomyosin system in the trabecular cells or inner wall endothelium of Schlemm's canal is an important factor in the regulation of outflow resistance. Cytoskeletal agents, affecting F-actin integrity or actomyosin contractility, or gene therapies, employing overexpression of caldesmon or Rho-A inhibition, can decrease outflow resistance in the drainage pathway. In this review, we discuss the mechanisms underlying these and similar effects on trabecular outflow resistance in living animals and/or in cultured ocular anterior segments from enucleated animal or human eyes.
Tian
Baohe
B
Department of Ophthalmology & Visual Sciences, University of Wisconsin, Madison, WI 53792-3220, USA.
Gabelt
B'Ann T
BT
Geiger
Benjamin
B
Kaufman
Paul L
PL
D000205:Actomyosin / Q000502:physiology*; D000818:Animals; D002148:Calmodulin-Binding Proteins / Q000494:pharmacology; D005902:Glaucoma, Open-Angle / Q000503:physiopathology; D006801:Humans; D007429:Intraocular Pressure / Q000187:drug effects / Q000502:physiology; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D014129:Trabecular Meshwork / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure; D050257:Tubulin Modulators / Q000494:pharmacology
D002148:Calmodulin-Binding Proteins; D047428:Protein Kinase Inhibitors; D050257:Tubulin Modulators; D000205:Actomyosin
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