Experimental eye research最新文献

{"title":"Functional characterization of CatTohm, a mouse AQP0 mutation that causes oxidative stress, cytotoxicity, dominant congenital lens cataract and microphthalmia","authors":"Sindhu Kumari ,&nbsp;Tadashi Okamura ,&nbsp;Kulandaiappan Varadaraj","doi":"10.1016/j.exer.2025.110434","DOIUrl":"10.1016/j.exer.2025.110434","url":null,"abstract":"<div><div>A natural AQP0 mutation, <em>Cat</em>^{<em>Tohm</em>}, resulted in smaller eyes, and lenses with bilateral dominant cataracts in mice. Our objective was to characterize this mutation and explore the possible reasons for <em>Cat</em>^Tohm causing dominant cataracts. We studied lens morphology, transparency, functional alterations and cytotoxicity. Lens morphology and nuclear fiber cell organization were severely affected. Water permeability (Pw) of oocytes expressing <em>Cat</em>^Tohm-AQP0 cRNA (12 ± 2 μm/s) reduced markedly (P &lt; 0001) compared with WT-cRNA-expressing oocytes (25 ± 2 μm/s); co-expression of both cRNAs decreased the Pw significantly (20 ± 3 μm/s; P &lt; 0.001). Pw of membrane vesicles of heterozygous (16 ± 4 μm/s), or homozygous (7 ± 3 μm/s) fiber cells was considerably lower (P &lt; 0.001) than that of the WT (37 ± 6 μm/s). The hydrogen peroxide permeability of the <em>Cat</em>^Tohm lens was remarkably lesser (P &lt; 0.0001) than that in the WT. The oxidative stress test revealed a significant (P &lt; 0.001) increase in Reactive Oxygen Species in <em>Cat</em>^{<em>Tohm</em> lenses}. In oocytes and cultured cells, transfected WT-AQP0 trafficked and expressed at the plasma membranes; mutant <em>Cat</em>^Tohm-AQP0 protein remained in the cytoplasm, and partly co-localized with the WT-AQP0. Cells transfected with <em>Cat</em>^Tohm-AQP0 showed more necrosis than apoptosis. The cultured cells expressing mutant AQP0, or <em>ex vivo</em> cultured lenses of <em>Cat</em>^Tohm displayed a substantial (P &lt; 0.001) rise in the discharge of lactate dehydrogenase in the culture medium, corroborating necrosis. A transgenic mouse lens expressing <em>Cat</em>^Tohm mutant AQP0 along with the WT-AQP0 had more severe microphthalmia than that of <em>Cat</em>^Tohm mouse. Overall, the <em>Cat</em>^Tohm mutation exerted a dominant negative effect affecting protein localization and functionality, and causing cellular stress, necrosis, lens cataracts and microphthalmia.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110434"},"PeriodicalIF":3.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144115466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lycium barbarum glycopeptide reduces inflammation and fibrosis in corneal injury by modulating the NF-κB/NLRP3/IL-1 β signaling pathway and microRNA-21a-5p/SMAD7","authors":"Yarong Yan ,&nbsp;Shulei Xing ,&nbsp;Jinghua Liu ,&nbsp;Xinlin Yan ,&nbsp;Yi Guan ,&nbsp;Zhixin Jiang ,&nbsp;Wei Zhang ,&nbsp;Xuan Li","doi":"10.1016/j.exer.2025.110438","DOIUrl":"10.1016/j.exer.2025.110438","url":null,"abstract":"<div><div>Lycium barbarum glycopeptide (LbGp), derived from the Chinese medicinal plant Lycium barbarum, has demonstrated anti-inflammatory properties; however, its precise role and mechanism in corneal repair following injury remain elusive. The present research investigated the mechanisms and effects of LbGp on corneal repair following alkali burn injury using in vivo mouse models of corneal alkali burn and in vitro human keratocyte fibrosis models. Corneal inflammation, opacity, and epithelial defects were assessed via a slit lamp microscope. Results showed that LbGp-treated mice exhibited reduced edema, accelerated re-epithelialization, and decreased corneal opacity compared to the phosphate-buffered saline (PBS)-treated controls. Proteomic analysis revealed altered proteins enriched in the extracellular matrix among the control, injury, and LbGp treatment groups. Moreover, LbGp significantly attenuated TGFβ-1-induced myofibroblasts transdifferentiation from keratocytes. Consistently, LbGp treatment inhibited the upregulation of fibrosis markers (αSMA, fibronectin, and collagen III) at both the protein and mRNA levels after corneal alkali burns. LbGp also effectively suppressed the activation of the NF-κB/NLRP3/IL-1β signaling pathway and neutrophil infiltration following corneal alkali burn injury. Additionally, miR-21 was upregulated in TGFβ-1-stimulated keratocytes and in the alkali-burned mouse cornea. LbGp decreased miR-21 expression, while increasing expression of its target, Smad7, thereby dampening the TGFβ/Smad2/3 signaling pathway. This research demonstrates that LbGp promotes corneal healing by inhibiting inflammation and fibrosis after alkali burns, suggesting its potential as a supplementary therapy for corneal injury repair.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110438"},"PeriodicalIF":3.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PINK1-mediated mitochondrial autophagy protects lens epithelial cells by reducing ROS and apoptosis","authors":"Xiangyu Liu ,&nbsp;Meiyu Wang ,&nbsp;Zhenzhen Ji ,&nbsp;Xuanlin Zhu,&nbsp;Jinchang Tian,&nbsp;Yingxin Chen,&nbsp;Jun Cai,&nbsp;Mei Dong,&nbsp;Zhijian Li","doi":"10.1016/j.exer.2025.110437","DOIUrl":"10.1016/j.exer.2025.110437","url":null,"abstract":"<div><div>Cataracts are one of the primary causes of blindness worldwide; however, their pathogenesis remains unclear. Oxidative stress and apoptosis are two dominant inducers in the progression of cataracts; however, little is known about the specific mechanisms associated with mitophagy. This study aimed to investigate the role of PTEN-induced putative kinase 1(PINK1)-mediated mitophagy in cataract development. Initially, we induced a rat cataract model using sodium selenite and observed the upregulated expression of PINK1 and other autophagy-related proteins within lens epithelial cells, accompanied by apoptosis. Furthermore, the survival rate of human lens epithelial cells was significantly reduced by H₂O₂ treatment. However, PINK1 overexpression reduced ROS levels, allowing cells to survive. This reduction in reactive oxygen species (ROS) levels led to a decrease in cleaved caspase-3 and Bcl-2-associated X protein (Bax) expression and an increase in B-cell lymphoma 2 (Bcl-2) levels. In summary, PINK1 maintains mitochondrial functional stability and inhibits apoptosis by activating mitophagy, thus potentially playing a crucial protective role in cataract pathogenesis.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"258 ","pages":"Article 110437"},"PeriodicalIF":3.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantifying retinal oxygenation and metabolism by phosphorescence lifetime imaging","authors":"Mahnaz Shahidi","doi":"10.1016/j.exer.2025.110422","DOIUrl":"10.1016/j.exer.2025.110422","url":null,"abstract":"<div><div>The retina is a highly metabolically active tissue, requiring adequate availability of oxygen and other metabolites to generate energy for cellular survival and visual function. Retinal hypoxia has been implicated in several common retinal diseases and associated with the development of vision-threatening pathologies. Since the level of hypoxia determines processes that are activated for either cell survival or death, knowledge of retinal oxygenation is essential. This article reviews depth-resolved quantitative measurements of retinal vascular and tissue oxygen tension in rodents using the technique of phosphorescence lifetime imaging. Furthermore, retinal oxygen metabolic biomarkers were quantitatively derived from oxygen tension measurements and shown to be altered under challenged physiological and pathological conditions. Application of phosphorescence lifetime imaging can be useful for advancing knowledge of retinal ischemia pathophysiology and identifying physiological biomarkers to monitor progression and evaluate therapeutic interventions in animal models of human retinal diseases.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110422"},"PeriodicalIF":3.0,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A multiomic study of retinal tissues in mice with direct ocular exposure to vesicants","authors":"Assylbek Zhylkibayev ,&nbsp;James Mobley ,&nbsp;Mohammad Athar ,&nbsp;Marina Gorbatyuk","doi":"10.1016/j.exer.2025.110414","DOIUrl":"10.1016/j.exer.2025.110414","url":null,"abstract":"<div><div>This study employed a multiomic approach to investigate retinal tissue damage following direct ocular exposure (DOE) to vesicants (VSs)—namely, nitrogen mustard (NM) and lewisite (Lew). We explored both the acute and chronic stages of retinal injury by assessing functional, structural, and molecular changes. C57BL/6 mice were used to measure scotopic and photopic electroretinograms (ERGs) and to analyze TUNEL-positive retinal cells. Global retinal proteomics was conducted to identify common and unique signaling pathways. In addition, we performed targeted metabolomic and lipidomic analyses of retinal tissue to uncover significant metabolic changes. Our results demonstrated remarkable declines in ERG amplitudes at 2 and 4 weeks post-exposure, accompanied by an increase in TUNEL⁺ retinal cells in response to DOE to both VSs. Our proteomic analysis revealed chronic oxidative stress, mitochondrial dysfunction, elevated RXR signaling, and increased levels of 28 proteins. Moreover, we observed a decline in the KEGG phototransduction pathways, along with the downregulation of photoreceptor-specific proteins, in response to both VSs. Consistent with the proteomic findings, targeted metabolomics identified a decline in phototransduction and steroid hormone biosynthesis, along with increases in D-amino acid and purine metabolism, as well as lysine degradation. These changes were associated with a GSSG/GSH ratio of 2.6, confirming the proteomic data on oxidative stress. Furthermore, lipidomic analysis revealed an increase in oxidative lipid levels, accompanied by a 3.4-fold increase in phosphatidylserine (PS), suggesting apoptotic cell death and a reduction in fatty acids (FAs). In conclusion, exposure to both VSs induced progressive retinal damage, altering major metabolic pathways and dysregulating lipid metabolism. Future studies should focus on identifying the responses of individual neuronal cell types to DOE to VSs to develop cell-specific countermeasures.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110414"},"PeriodicalIF":3.0,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144071216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identifying a role for oxytosis/ferroptosis in Pde6b-associated retinitis pigmentosa","authors":"Madison E. Weiss ,&nbsp;Paola E. Parrales ,&nbsp;Maumita Datta ,&nbsp;Michelle Fleishaker ,&nbsp;Galina Gvoriantchikova ,&nbsp;Dmitry Ivanov ,&nbsp;Abigail S. Hackam","doi":"10.1016/j.exer.2025.110424","DOIUrl":"10.1016/j.exer.2025.110424","url":null,"abstract":"<div><div>Inherited retinal diseases (IRDs) are a large heterogeneous group of diseases that lead to visual impairment and complete vision loss. Retinitis pigmentosa (RP) is an IRD with progressive degeneration of photoreceptors and has been associated with mutations in over 80 genes. In this study, we investigated the mechanism of retinal degeneration caused by an inherited mutation in the <em>Pde6b</em> gene in the <em>rd10</em> mouse model of RP, with a focus on alternative programmed cell death pathways. RNA-seq analysis was used to identify changes in gene expression in <em>rd10</em> mice, using C57BL/6J mice as non-degenerating genetic background controls. The functional role of differentially expressed genes was investigated using pharmacological treatments and visual acuity was assessed using optomotor kinetic tracking assay. We found increased expression of genes involved in inflammatory response, while expression of genes involved in photoreceptor function and homeostasis were decreased. We also demonstrated increased expression of genes that regulate oxytosis/ferroptosis, a type of regulated necrosis that can promote inflammatory responses. We found no significant changes in expression of genes controlling other types of regulated necrosis. Treating <em>rd10</em> mice with oxytosis/ferroptosis inhibitors led to significant improvements in visual acuity. Therefore, these findings suggest that disruption of <em>Pde6b</em> activity results in photoreceptor death via oxytosis/ferroptosis, contributing to inflammatory responses in the retina. Our results identify for the first time a possible role of oxytosis/ferroptosis in a model of inherited retinal degeneration and provide a foundation for further studies exploring oxytosis/ferroptosis inhibitors as a potential therapeutic strategy for RP.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110424"},"PeriodicalIF":3.0,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144072228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the link between Co-stimulatory gene polymorphisms and clinical manifestations in Graves' ophthalmopathy","authors":"Ding-Ping Chen ,&nbsp;Chia-Rui Shen ,&nbsp;Wei-Tzu Lin ,&nbsp;Yen-Chang Chu","doi":"10.1016/j.exer.2025.110423","DOIUrl":"10.1016/j.exer.2025.110423","url":null,"abstract":"<div><div>Graves' ophthalmopathy (GO) is an autoimmune disorder that affects orbital tissues in approximately 30 % of Graves' disease patients. Single nucleotide polymorphisms (SNPs), particularly in immune-related genes, play a crucial role in the development of GO. This study investigates the association between SNPs in co-stimulatory molecules and specific clinical characteristics of GO, including laterality, orbital pain, swelling, diplopia, exophthalmos, redness, and eyelid retraction. Forty-one patients newly diagnosed with GO were analyzed. Genomic DNA was extracted from their blood, and 98 SNPs were amplified using PCR and sequenced. Candidate SNPs, selected based on prior research, were analyzed using chi-square tests and genetic models to assess genotype and allele frequency differences related to clinical manifestations. CD28 SNPs rs3181096 (C vs. T: p = 0.001) and rs3181098 (G vs. A: p = 0.002) were found to show protective effects against eyelid inflammation, while the A-allele of rs200353921(p = 0.005) increased the risk of eyelid inflammation. PDCD1 SNPs rs36084323 (C vs. T: p = 0.004) and rs41386349 (G vs. A: p = 0.005) were linked to diplopia and eyelid inflammation, respectively. The T-allele of rs6705653 in PDCD1 was found to increase the risk of diplopia (p = 0.001) but decreased the risk of eyelid retraction (p = 0.002). Other SNPs, including rs2227982 (p = 0.003) and rs2227981 (G vs. A: p = 0.001), were also associated with diplopia and eyelid retraction, highlighting the complex genetic influences on the clinical manifestations of GO. Furthermore, interactions between age, gender, and SNPs were observed in relation to GO clinical features. These findings highlight the potential regulatory roles of these genes in influencing immune responses and orbital inflammation in GO. Understanding these genetic influences could help identify predictive markers and novel therapeutic targets for GO management.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110423"},"PeriodicalIF":3.0,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Grx2 maintains GSH/GSSG homeostasis to enhance GPX4-mediated ferroptosis defense in UVB irradiation induced cataract","authors":"Chenjun Guo ,&nbsp;Yong Guo ,&nbsp;Jie Zhang ,&nbsp;Jue Wang ,&nbsp;Liping Su ,&nbsp;Xiaona Ning ,&nbsp;Xi Chen ,&nbsp;Hong Yan","doi":"10.1016/j.exer.2025.110421","DOIUrl":"10.1016/j.exer.2025.110421","url":null,"abstract":"<div><h3>Purpose</h3><div>Ultraviolet B (UVB) irradiation induces cataract pathogenesis, and Glutaredoxin 2 (Grx2) deficiency causes the early onset of UVB-induced cataracts. Several researchers have shown that, apart from apoptosis and pyroptosis, UVB irradiation also can induce cell ferroptosis. We explored the role of ferroptosis caused by UVB irradiation in human lens epithelial cells (HLECs) and clarified how Grx2 protects against UVB-induced cataracts.</div></div><div><h3>Methods</h3><div>HLE-B3 cells and mice lenses were treated with DMSO or ferroptosis inhibitors after various doses of UVB irradiation. Cell morphology and ultrastructure were observed by optical microscope and transmission electron microscopy. Lens opacity was observed <em>ex vivo</em> using an optical microscope and <em>in vivo</em> using a slit lamp. The lipid peroxidation level was measured by C11-BODIPY probe and 4-HNE (the lipid peroxidation marker) protein expression. Cell viability was determined using the CCK-8 kit and propodium iodide (PI) immunofluorescence. Grx2 KO and KI mice, Grx2 silencing and Grx2 overexpression in HLE-B3 cell lines were used for <em>in vivo</em> and <em>in vitro</em> experiments respectively.</div></div><div><h3>Results</h3><div>UVB-caused HLE-B3 cells death, lens opacity and lipid peroxidation could be mitigated by ferroptosis inhibitors. Grx2 KO mice accelerate the appearance of lens opacity induced by UVB. Meanwhile, Grx2 silencing enhanced HLECs lipid peroxidation susceptibility, downregulated the GSH level, shrunk mitochondria, and reduced the number of cristae. Grx2 overexpression had opposite effects.</div></div><div><h3>Conclusions</h3><div>Ferroptosis appears involved in UVB-induced HLECs damage. Inhibiting ferroptosis prevented UVB-induced cataracts. Grx2 strengthens resistance to ferroptosis induced by UVB irradiation through maintaining HLEC cellular GSH/GSSG homeostasis.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110421"},"PeriodicalIF":3.0,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Depletion of Polypyrimidine tract binding protein 1 (ptbp1) activates Müller glia-derived proliferation during zebrafish retina regeneration via modulation of the senescence secretome","authors":"Gregory J. Konar ,&nbsp;Audrey L. Lingan ,&nbsp;Kyle T. Vallone,&nbsp;Tu D. Nguyen,&nbsp;Zachary R. Flickinger,&nbsp;James G. Patton","doi":"10.1016/j.exer.2025.110420","DOIUrl":"10.1016/j.exer.2025.110420","url":null,"abstract":"<div><div>Polypyrimidine Tract Binding protein 1 (PTB) is an alternative splicing factor linked to neuronal induction and maturation. Previously, knockdown experiments supported a model in which PTB can function as a potent reprogramming factor, able to elicit direct glia-to-neuron conversion <em>in vivo</em>, in both the brain and retina<em>.</em> However, later lineage tracing and genetic knockouts of PTB did not support direct neuronal reprogramming. Nevertheless, consistent with the PTB depletion experiments, we show that antisense knockdown of PTB (<em>ptbp1a</em>) in the zebrafish retina can activate Müller glia-derived proliferation and that depletion of PTB can further enhance proliferation when combined with acute NMDA damage. The effects of PTB are consistent with a role in controlling key senescence and pro-inflammatory genes that are part of the senescence secretome that initiates retina regeneration.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110420"},"PeriodicalIF":3.0,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143942769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A standardized in vivo protocol for ocular biodistribution of gold nanoparticles","authors":"Alexis Loiseau ,&nbsp;Christelle Gross ,&nbsp;Sylvain Guérin ,&nbsp;Élodie Boisselier","doi":"10.1016/j.exer.2025.110409","DOIUrl":"10.1016/j.exer.2025.110409","url":null,"abstract":"<div><div>Effective drug administration plays a pivotal role in the treatment of eye diseases. Each route of ocular administration has its advantages and limitations, but a common challenge is the low bioavailability of drugs at the target sites. New delivery nanosystems are required to ensure sufficient drug concentration over time at the target in order to improve therapeutic efficacy. Gold nanoparticles represent a promising strategy for improving drug delivery to the eye, but they can be difficult to track in biological systems. To optimize the formulations, it is crucial to understand the biodistribution profiles of nanoparticles in the eye. Designing, interpreting and compiling research on the ocular biodistribution of nanoparticles raise major challenges, particularly considering the various nanoparticle-based ocular delivery systems and the multiple available animal models. The <em>in vivo</em> spatiotemporal distribution of nanoparticles in the eye is generally measured at specific time points after animal euthanasia and eye collection. In this technical article, we propose a detailed standardization of <em>in vivo</em> protocols for ocular biodistribution studies of gold-based delivery systems in rabbits following topical application. The protocol covers all steps, including enucleation, eye dissection of various ocular tissues and their digestion, as well as <em>ex vivo</em> analysis of gold (Au) atom content from gold nanoparticles by inductively coupled plasma-mass spectrometry (ICP-MS) at specific time points.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"257 ","pages":"Article 110409"},"PeriodicalIF":3.0,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}