Galectin-8 Promotes Cytoskeletal Rearrangement in Trabecular Meshwork Cells through Activation of Rho Signaling

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dc.contributor.authorDiskin, Shiri
dc.contributor.authorChen, Wei Sheng
dc.contributor.authorCao, Zhiyi
dc.contributor.authorGyawali, Smita
dc.contributor.authorGong, Haiyan
dc.contributor.authorSoza, Andrea
dc.contributor.authorGonzalez, Alfonso
dc.contributor.authorPanjwani, Noorjahan
dc.date.accessioned2024-01-10T13:48:41Z
dc.date.available2024-01-10T13:48:41Z
dc.date.issued2012
dc.description.abstractPurpose: The trabecular meshwork (TM) cell-matrix interactions and factors that influence Rho signaling in TM cells are thought to play a pivotal role in the regulation of aqueous outflow. The current study was designed to evaluate the role of a carbohydrate-binding protein, galectin-8 (Gal8), in TM cell adhesion and Rho signaling.
dc.description.abstractMethods: Normal human TM cells were assayed for Gal8 expression by immunohistochemistry and Western blot analysis. To assess the role of Gal8 in TM cell adhesion and Rho signaling, the cell adhesion and spreading assays were performed on Gal8-coated culture plates in the presence and the absence of anti-beta(1) integrin antibody and Rho and Rho-kinase inhibitors. In addition, the effect of Gal8-mediated cell-matrix interactions on TM cell cytoskeleton arrangement and myosin light chain 2 (MLC2) phosphorylation was examined.
dc.description.abstractPrincipal Findings: We demonstrate here that Gal8 is expressed in the TM and a function-blocking anti-beta(1) integrin antibody inhibits the adhesion and spreading of TM cells to Gal8-coated wells. Cell spreading on Gal8 substratum was associated with the accumulation of phosphorylated myosin light chain and the formation of stress fibers that was inhibited by the Rho inhibitor, C3 transferase, as well as by the Rho-kinase inhibitor, Y27632.
dc.description.abstractConclusions/Significance: The above findings present a novel function for Gal8 in activating Rho signaling in TM cells. This function may allow Gal8 to participate in the regulation of aqueous outflow.
dc.description.funderNational Institutes of Health
dc.description.funderResearch to Prevent Blindness
dc.description.funderFONDECYT (National Fund for Scientific and Technological Development)
dc.description.funderFONDAP (Fund for Advanced Research in Priority Areas (Centers of Excellence FONDAP)
dc.description.funderNATIONAL EYE INSTITUTE
dc.format.extent10 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1371/journal.pone.0044400
dc.identifier.issn1932-6203
dc.identifier.pubmedidMEDLINE:22973445
dc.identifier.urihttps://doi.org/10.1371/journal.pone.0044400
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/79388
dc.identifier.wosidWOS:000308577600049
dc.information.autorucMedicina;Gonzalez A ;S/I;52306
dc.information.autorucMedicina;Soza A ;S/I;129570
dc.issue.numero9
dc.language.isoen
dc.nota.accesoSin adjunto
dc.publisherPUBLIC LIBRARY SCIENCE
dc.revistaPLOS ONE
dc.rightsregistro bibliográfico
dc.subjectAQUEOUS-HUMOR OUTFLOW
dc.subjectOPEN-ANGLE GLAUCOMA
dc.subjectKINASE INHIBITOR
dc.subjectPROTEIN-KINASE
dc.subjectBETA(1) INTEGRIN
dc.subjectCYTOCHALASIN-B
dc.subjectADHESION
dc.subjectFACILITY
dc.subjectFIBRONECTIN
dc.subjectEXPRESSION
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleGalectin-8 Promotes Cytoskeletal Rearrangement in Trabecular Meshwork Cells through Activation of Rho Signaling
dc.typeartículo
dc.volumen7
sipa.codpersvinculados52306
sipa.codpersvinculados129570
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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