http://purl.uniprot.org/citations/22064993 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/22064993 | http://www.w3.org/2000/01/rdf-schema#comment | "PurposeTo examine the functional significance of EphB/ephrin-B upregulation in mouse experimental glaucoma.MethodsIn a loss-of-function approach, mouse mutants lacking EphB2 (EphB2(-/-)) or EphB3 (EphB3(-/-)) protein, and mutants expressing EphB2 truncated in the C-terminus (EphB2(lacZ/lacZ)) were subjected to laser-induced ocular hypertension (LIOH), an experimental mouse model of glaucoma. The number of optic nerve axons was counted in paraphenylenediamine (PPD)-stained sections and compared between EphB mutants and wild type littermates. In a gain-of-function approach, retina/optic nerve explants obtained from LIOH-treated animals were exposed to EphB2-Fc recombinant proteins or Fc control proteins. Tissue sections through the optic nerve head (ONH) were labeled with neuron-specific anti-tubulin β-III antibody to determine axonal integrity.ResultsBoth EphB2 and EphB3 null mutant mice exhibited more severe axonal degeneration than wild type littermates after treatment with LIOH. Mutant mice in which the C-terminal portion of EphB2 is truncated had an intermediate phenotype. Application of EphB2-Fc recombinant protein to LIOH-treated optic nerve explants resulted in greater sparing of tubulin β-III-containing retinal ganglion cell (RGC) axons.ConclusionsThese results provide genetic evidence in mice that both EphB/ephrin-B forward and reverse signaling feed into an endogenous pathway to moderate the effects of glaucomatous insult on RGC axons. LIOH-induced axon loss is maintained in retina/optic nerve explants after removal from an ocular hypertensive environment. Exogenous application of EphB2 protein enhances RGC axon survival in explants, suggesting that modulation of Eph/ephrin signaling may be of therapeutic interest."xsd:string |
http://purl.uniprot.org/citations/22064993 | http://purl.org/dc/terms/identifier | "doi:10.1167/iovs.11-8546"xsd:string |
http://purl.uniprot.org/citations/22064993 | http://purl.uniprot.org/core/author | "Sretavan D."xsd:string |
http://purl.uniprot.org/citations/22064993 | http://purl.uniprot.org/core/author | "Fu C.T."xsd:string |
http://purl.uniprot.org/citations/22064993 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
http://purl.uniprot.org/citations/22064993 | http://purl.uniprot.org/core/name | "Invest Ophthalmol Vis Sci"xsd:string |
http://purl.uniprot.org/citations/22064993 | http://purl.uniprot.org/core/pages | "76-84"xsd:string |
http://purl.uniprot.org/citations/22064993 | http://purl.uniprot.org/core/title | "Involvement of EphB/Ephrin-B signaling in axonal survival in mouse experimental glaucoma."xsd:string |
http://purl.uniprot.org/citations/22064993 | http://purl.uniprot.org/core/volume | "53"xsd:string |
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