ArticleFrontiers in molecular neuroscience2016
Increased Expression of Osteopontin in Retinal Degeneration Induced by Blue Light-Emitting Diode Exposure in Mice.
Article in Frontiers in molecular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Determination of osteopontin in monitoring retinal damage in metabolic syndrome.International journal of experimental pathology · 2024Article
- Changes in Retinal Structure and Function in Mice Exposed to Flickering Blue Light: Electroretinographic and Optical Coherence Tomographic Analyses.Experimental neurobiology · 2024Article
- An Update to Biomechanical and Biochemical Principles of Retinal Injury in Child Abuse.Children (Basel, Switzerland) · 2024Review
- Immunoregulatory Roles of Osteopontin in Diseases.Nutrients · 2024Review
- A Distinct Microglial Cell Population Expressing Both CD86 and CD206 Constitutes a Dominant Type and Executes Phagocytosis in Two Mouse Models of Retinal Degeneration.International journal of molecular sciences · 2023Article
- Patterns of NFkB activation resulting from damage, reactive microglia, cytokines, and growth factors in the mouse retina.Experimental neurology · 2023Article
- Short- and Long-Term Study of the Impact of Focal Blue Light-Emitting Diode-Induced Phototoxicity in Adult Albino Rats.International journal of molecular sciences · 2021Article
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- Plasma biomarkers of the amyloid pathway are associated with geographic atrophy secondary to age-related macular degeneration.PloS one · 2020Article
- Effects of Different Light Sources on Neural Activity of the Paraventricular Nucleus in the Hypothalamus.Medicina (Kaunas, Lithuania) · 2019Article
- Osteopontin and its spatiotemporal relationship with glial cells in the striatum of rats treated with mitochondrial toxin 3-nitropropionic acid: possible involvement in phagocytosis.Journal of neuroinflammation · 2019Article
- Ocular hazards of curing light units used in dental practice - A systematic review.The Saudi dental journal · 2019Review
- Development of a Post-vitrectomy Injection of N-methyl-N-nitrosourea as a Localized Retinal Degeneration Rabbit Model.Experimental neurobiology · 2019Article
- Amelioration of Mouse Retinal Degeneration After Blue LED Exposure by Glycyrrhizic Acid-Mediated Inhibition of Inflammation.Frontiers in cellular neuroscience · 2019Article
- The Retina of Osteopontin deficient Mice in Aging.Molecular neurobiology · 2018Article
- The Effect of Osteopontin on Microglia.BioMed research international · 2017Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteopontin (OPN) is a multifunctional adhesive glycoprotein that is implicated in a variety of pro-inflammatory as well as neuroprotective and repair-promoting effects in the brain. As a first step towards understanding the role of OPN in retinal degeneration (RD), we examined changes in OPN expression in a mouse model of RD induced by exposure to a blue light-emitting diode (LED). RD was induced in BALB/c mice by exposure to a blue LED (460 nm) for 2 h. Apoptotic cell death was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. In order to investigate changes in OPN in RD, western blotting and immunohistochemistry were performed. Anti-OPN labeling was compared to that of anti-glial fibrillary acidic protein (GFAP), which is a commonly used marker for retinal injury or stress including inflammation. OPN expression in RD retinas markedly increased at 24 h after exposure, was sustained through 72 h, and subsided at 120 h. Increased OPN expression was observed co-localized with microglial cells in the outer nuclear layer (ONL), outer plexiform layer (OPL), and subretinal space. Expression was restricted to the central retina in which photoreceptor cell death occurred. Interestingly, OPN expression in the ONL/OPL was closely associated with microglia, whereas most of the OPN plaques observed in the subretinal space were not. Immunogold electron microscopy demonstrated that OPN was distributed throughout the cytoplasm of microglia and in nearby fragments of degenerating photoreceptors. In addition, we found that OPN was induced more acutely and with greater region specificity than GFAP. These results indicate that OPN may be a more useful marker for retinal injury or stress, and furthermore act as a microglial pro-inflammatory mediator and a phagocytosis-inducing opsonin in the subretinal space. Taken together, our data suggest that OPN plays an important role in the pathogenesis of RD.
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