Increased Expression of Osteopontin in Retinal Degeneration Induced by Blue Light-Emitting Diode Exposure in Mice

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.

Development of a Post-vitrectomy Injection of N-methyl-N-nitrosourea as a Localized Retinal Degeneration Rabbit Model

“…5). GFAP staining shows expression at the end feet of Müller cells and expression increases in retinal injury or inflammatory conditions, therefore, GFAP is a representative marker for retinal injury or stress [33]. In our study, GFAP staining was increased in both the non-degenerated and degenerated areas in the ganglion cell, inner plexiform, and inner nuclear layers, and it seems that the performance of vitrectomy and intravitreal injection caused retinal stress and induced fibrosis and proliferation of glial cells, regardless of degeneration [34].…”

The Retina of Osteopontin deficient Mice in Aging

“…Reactive astrocytes express OPN following different types of brain insult [ 19 – 21 ], and it has also been associated with the microglia that fulfill macrophagic functions [ 18 ]. As occurs in astrocytes, OPN is upregulated in activated microglia after CNS damage [ 22 – 27 ], suggesting that it may play a key role in the pathogenesis of neuroinflammation [ 20 ]. OPN binds to the integrin αvβ3 receptor, which means it may act as a chemoattractant in recruiting astrocytes and microglia during the formation of the glial scar following ischemic injury [ 20 , 23 , 24 , 28 , 29 ].…”

Ocular hazards of curing light units used in dental practice – A systematic review

“…All articles in this review (Jiangmei et al, 1999, McCusker et al, 2013, Labrie et al, 2011, Rassaei et al, 2013, Price et al, 2016, Chang et al, 2016, Lee et al, 2016) are in-vitro experimental except one (Eriksen et al, 1987) which is an in-vivo experimental study. Three studies (Jiangmei et al, 1999, Chang et al, 2016, Lee et al, 2016) were conducted on live rodents (rats and mice) while one study (Rassaei et al, 2013) employed bovine superfused retina. One study (Price et al, 2016) used human teeth model while another study (Labrie et al, 2011) used extracted human maxillary teeth.…”