Exogenous modulation of intrinsic optic nerve neuroprotective activity

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dc.contributor.authorGrozdanic, Sinisa D.
dc.contributor.authorLazic, Tatjana
dc.contributor.authorKuehn, Markus H.
dc.contributor.authorHarper, Matthew M.
dc.contributor.authorKardon, Randy H.
dc.contributor.authorKwon, Young H.
dc.contributor.authorLavik, Erin
dc.contributor.authorSakaguchi, Donald S.
dc.date.accessioned2025-06-17T14:46:40Z
dc.date.available2025-06-17T14:46:40Z
dc.date.issued2010-08-01
dc.description.abstractBackgroundTo characterize the molecular and functional status of the rat retina and optic nerve after acute elevation of intraocular pressure (IOP).MethodsRetinal ischemia was induced in rats by increasing the IOP (110 mmHg/60 minutes). Microarray analysis, quantitative RT-PCR (qRT-PCR) and immunohistochemistry were used to characterize retinal tissue. PLGA microspheres containing neurotrophic factors (BDNF, GDNF, or CNTF) or empty microspheres were injected into the vitreous of operated animals 1 day after elevation of IOP. Pupil light reflex (PLR) parameters and electroretinograms (ERG) were monitored at multiple time points during the 60-day postoperative recovery period.ResultsMolecular analysis showed a significant intrinsic up-regulation of CNTF at 10 and 25 days after induction of the acute ocular hypertension (p=0.0067). Molecular tissue analysis of GDNF and its receptors (GDNFR1, GDNFR2), and BDNF and its receptor (trkB) showed no change in expression. Animals that received CNTF microspheres had no significant functional recovery compared to animals which received blank microspheres (p>0.05). Animals that received GDNF or BDNF microspheres showed significant PLR recovery (p<0.05 and p<0.001 respectively) compared to non-treated animals.ConclusionsContinuous release of neurotrophic growth factors (NGFs) significantly protects optic nerve function in the experimental model of retinal ischemia observed by PLR analysis.
dc.description.sponsorshipThis work was supported in part by Department of Veterans Affairs Veterans Health Administration Rehabilitation Research and Development Service Grant C3919R The Glaucoma Foundation NY an unrestricted grant from Research to Prevent Blindness Dept of Ophthalmology University of Iowa NIH NS044007 NIH EY019485 NIH EY019294 and ISU Biotechnology Carver Trust Grant
dc.description.urihttps://link.springer.com/article/10.1007/s00417-010-1336-7
dc.format.extent23 pages
dc.genrejournal articles
dc.genrepostprints
dc.identifierdoi:10.13016/m2mrph-69fz
dc.identifier.citationGrozdanic, Sinisa D., Tatjana Lazic, Markus H. Kuehn, Matthew M. Harper, Randy H. Kardon, Young H. Kwon, Erin B. Lavik, and Donald S. Sakaguchi. “Exogenous Modulation of Intrinsic Optic Nerve Neuroprotective Activity.” Graefe’s Archive for Clinical and Experimental Ophthalmology 248, no. 8 (August 1, 2010): 1105–16. https://doi.org/10.1007/s00417-010-1336-7.
dc.identifier.urihttps://doi.org/10.1007/s00417-010-1336-7
dc.identifier.urihttp://hdl.handle.net/11603/39066
dc.language.isoen_US
dc.publisherSpringer
dc.relation.isAvailableAtThe University of Maryland, Baltimore County (UMBC)
dc.relation.ispartofUMBC Chemical, Biochemical & Environmental Engineering Department
dc.relation.ispartofUMBC College of Engineering and Information Technology Dean's Office
dc.rightsThis version of the article has been accepted for publication, after peer review (when applicable) and is subject to Springer Nature’s AM terms of use, but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: http://dx.doi.org/10.1007/s00417-010-1336-7.
dc.subjectGDNF
dc.subjectRetina
dc.subjectBDNF
dc.subjectNeuroprotection
dc.subjectCNTF
dc.titleExogenous modulation of intrinsic optic nerve neuroprotective activity
dc.typeText
dcterms.creatorhttps://orcid.org/0000-0002-0644-744X

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