NDLI: Novel molecular insights into RhoA GTPase-induced resistance to aqueous humor outflow through the trabecular meshwork.

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Novel molecular insights into RhoA GTPase-induced resistance to aqueous humor outflow through the trabecular meshwork.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhang, Min Maddala, Rupalatha Rao, Ponugoti Vasantha
Description	Country affiliation: United States Author Affiliation: Zhang M ( Dept. of Ophthalmology, Duke Univ. School of Medicine, 2351 Erwin Rd., Durham, NC 27710, USA.)
Abstract	Impaired drainage of aqueous humor through the trabecular meshwork (TM) culminating in increased intraocular pressure is a major risk factor for glaucoma, a leading cause of blindness worldwide. Regulation of aqueous humor drainage through the TM, however, is poorly understood. The role of RhoA GTPase-mediated actomyosin organization, cell adhesive interactions, and gene expression in regulation of aqueous humor outflow was investigated using adenoviral vector-driven expression of constitutively active mutant of RhoA (RhoAV14). Organ-cultured anterior segments from porcine eyes expressing RhoAV14 exhibited significant reduction of aqueous humor outflow. Cultured TM cells expressing RhoAV14 exhibited a pronounced contractile morphology, increased actin stress fibers, and focal adhesions and increased levels of phosphorylated myosin light chain (MLC), collagen IV, fibronectin, and laminin. cDNA microarray analysis of RNA extracted from RhoAV14-expressing human TM cells revealed a significant increase in the expression of genes encoding extracellular matrix (ECM) proteins, cytokines, integrins, cytoskeletal proteins, and signaling proteins. Conversely, various ECM proteins stimulated robust increases in phosphorylation of MLC, paxillin, and focal adhesion kinase and activated Rho GTPase and actin stress fiber formation in TM cells, indicating a potential regulatory feedback interaction between ECM-induced mechanical strain and Rho GTPase-induced isometric tension in TM cells. Collectively, these data demonstrate that sustained activation of Rho GTPase signaling in the aqueous humor outflow pathway increases resistance to aqueous humor outflow through the trabecular pathway by influencing the actomyosin assembly, cell adhesive interactions, and the expression of ECM proteins and cytokines in TM cells.
File Format	HTM / HTML
ISSN	03636143
e-ISSN	15221563
DOI	10.1152/ajpcell.00481.2007
Journal	American Journal of Physiology - Cell Physiology
Issue Number	5
Volume Number	295
Language	English
Publisher	American Physiological Society
Publisher Date	2008-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Aqueous Humor Enzymology Cytoskeleton Trabecular Meshwork Rhoa Gtp-binding Protein Metabolism Actins Animals Cell Adhesion Cells, Cultured Cytokines Genetics Extracellular Matrix Proteins Focal Adhesions Gene Expression Profiling Gene Transfer Techniques Intraocular Pressure Mutation Myosin Light Chains Organ Culture Techniques Phosphorylation Stress Fibers Swine Time Factors Up-regulation
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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