Experimental eye research最新文献

{"title":"The hypoxia-mediated HIF-1α/miR-381-3p signaling pathway promotes retinal neovascularization","authors":"Qingguo Guo ,&nbsp;Xin Xu ,&nbsp;Qicheng Tian ,&nbsp;Haoran Zhu ,&nbsp;Lei Pei ,&nbsp;Guangzuo Luo ,&nbsp;Ying Liu","doi":"10.1016/j.exer.2026.110925","DOIUrl":"10.1016/j.exer.2026.110925","url":null,"abstract":"<div><div>Retinal neovascularization is a common pathological feature of various retinal vascular diseases and is typically induced by hypoxia. In recent studies, the regulatory role of microRNA (miRNA)-mediated signaling in retinal neovascularization has been extensively characterized. However, although hypoxia-induced miRNA dysregulation has been identified, the specific mechanisms by which hypoxia modulates miRNAs in retinal neovascularization remain largely elusive. In this study, we first established a direct regulatory link between microRNA-381-3p (miR-381-3p) and hypoxia-inducible factor-1α (HIF-1α) using a dual-luciferase reporter gene assay. Based on an <em>in vitro</em> cellular hypoxia model and an <em>in vivo</em> oxygen-induced retinopathy (OIR) mouse model, we validated the regulatory effect of HIF-1α on miR-381-3p expression. In addition, downregulation of miR-381-3p attenuated retinal neovascularization, inflammation, and apoptosis in OIR mice. Transcriptome sequencing analysis identified Steap4, a differentially expressed gene, as a potential downstream target of miR-381-3p. Further detection suggested that inhibition of miR-381-3p expression could down-regulate the expression of STEAP4 both <em>in vitro</em> and in <em>vivo</em>. Collectively, our study provides compelling evidence that the HIF-1α/miR-381-3p pathway plays a critical regulatory role in retinal neovascularization, which complements the pathogenic mechanisms underlying retinal vascular diseases and suggests that miR-381-3p may serve as a potential therapeutic target for treating retinal neovascularization.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110925"},"PeriodicalIF":2.7,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146178510","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":"Neurotrophin-4 as a promising therapy for corneal injuries: Enhancing epithelial repair and nerve regeneration in abrasion and alkali burn models","authors":"Dai Su ,&nbsp;Qiaoran Qi ,&nbsp;Jin Li ,&nbsp;Xuxiang Zhang","doi":"10.1016/j.exer.2026.110917","DOIUrl":"10.1016/j.exer.2026.110917","url":null,"abstract":"<div><div>Corneal injury and nerve degeneration are complex issues associated with various eye diseases, presenting significant challenges in the field of ophthalmology. Current treatment methods often fail to completely restore corneal nerve function and tissue integrity after injury, underscoring the urgent need for new regenerative strategies. Neurotrophin-4 (NT-4), a member of the neurotrophin family, exerts crucial roles in cell survival and tissue repair through binding to the TrkB receptor. This study investigates the therapeutic potential of NT-4 for corneal injury. In vitro experiments demonstrated that NT-4 enhanced the migration of corneal epithelial cells and axonal outgrowth of trigeminal ganglion cells, effects that were abrogated by the TrkB-specific inhibitor ANA-12. In mouse models, compared to control groups, NT-4 accelerated the healing of both corneal abrasions and alkali burns, elevated corneal nerve density, restored corneal transparency. These findings suggest that NT-4 plays a pivotal role in corneal epithelial repair and sensory nerve regeneration through TrkB-mediated mechanisms, supporting its potential as a therapeutic agent for managing ocular surface injuries.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110917"},"PeriodicalIF":2.7,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146178438","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":"Animal-based experimental models in dry eye research: Current approaches and limitations","authors":"Ilayda Korkmaz ,&nbsp;Melis Palamar","doi":"10.1016/j.exer.2026.110918","DOIUrl":"10.1016/j.exer.2026.110918","url":null,"abstract":"<div><div>Experimental animal models offer simplified yet highly controlled systems that enable the systematic exploration of the biological processes underlying human diseases. In dry eye disease (DED), animal models mimic the clinical and pathological features. A wide spectrum of approaches has been developed depending on the targeted mechanism, including aqueous-deficient, evaporative, and mucin-deficient models. Nevertheless, existing models fail to reproduce the multifactorial and heterogeneous nature of DED. Most models are highly useful for short-term evaluations; however, they are insufficient for long-term studies and fail to mimic the chronic course of the disease. Although aqueous-deficient DED models may be advantageous for inducing a more stable and severe DED phenotype, substantial interspecies variability can markedly influence the outcomes. Variability in the lacrimal apparatus, including divided glandular architecture and the presence of accessory glands, such as nictitating membranes and Harderian glands, may attenuate or compensate for the induced phenotype and limit model robustness. Evaporative DED models offer practical advantages and rapid induction but produce only mild ocular surface changes, not reflecting the chronic form of human diseases. A combination of multiple induction methods may yield more comprehensive and physiologically relevant models. In addition to these challenges, the human-oriented design of most diagnostic tests introduces uncertainties in protocol adaptation, optimal thresholds, and interpretation. This review summarizes the key methodologies, diagnostic considerations, advantages, and limitations of the available DED models, while highlighting persistent gaps that constrain their translational relevance.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110918"},"PeriodicalIF":2.7,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146178498","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":"Response to comments on “Circadian rhythm disruption induces myopia in mice”","authors":"Wei-Ling Bai ,&nbsp;Mei-Jun Wang ,&nbsp;Jia-He Gan ,&nbsp;Ying Huang ,&nbsp;Zi-Han Liu ,&nbsp;Cong-Ying Li ,&nbsp;Ning-Li Wang ,&nbsp;Shi-Ming Li","doi":"10.1016/j.exer.2026.110889","DOIUrl":"10.1016/j.exer.2026.110889","url":null,"abstract":"","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110889"},"PeriodicalIF":2.7,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146156478","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":"Role of NDUFS1 in mitochondrial dysfunction and oxidative stress in glaucomatous retinal ganglion cells","authors":"Jing Zhang ,&nbsp;Lin Jiang ,&nbsp;Xiao Zheng","doi":"10.1016/j.exer.2026.110913","DOIUrl":"10.1016/j.exer.2026.110913","url":null,"abstract":"<div><div>This study investigates the role of NDUFS1, a subunit of mitochondrial complex I, in glaucomatous retinal ganglion cell (RGC) injury and determines whether it mediates RGC apoptosis through regulating mitochondrial dysfunction and oxidative stress (OS). A microbead-induced glaucoma mouse model was established. Intraocular pressure (IOP) measurements, retinal whole-mount immunofluorescence staining, TUNEL assay, and OS marker detection were conducted to assess RGC survival, apoptosis, and OS. <em>In vitro</em>, NDUFS1 was knocked down or overexpressed in R28 retinal cells. JC-1 staining, adenosine triphosphate (ATP) assay, and flow cytometry were employed to analyze the impacts of NDUFS1 on mitochondrial membrane potential, energy metabolism, OS, and apoptosis. Finally, adeno-associated virus-mediated NDUFS1 overexpression (AAV-oe-NDUFS1) was delivered via intravitreal injection to validate its protective effects <em>in vivo</em>. <em>In vivo</em> experiments revealed downregulation of NDUFS1 expression in the retinas of glaucoma mice, accompanied by significant RGC loss, enhanced OS, and increased apoptosis. <em>In vitro</em>, NDUFS1 knockdown induced mitochondrial membrane depolarization, reduced ATP synthesis, exacerbated OS, and ultimately promoted apoptosis. Conversely, NDUFS1 overexpression effectively reversed these pathological phenotypes. Rescue experiments <em>in vivo</em> further demonstrated that NDUFS1 upregulation alleviated OS, suppressed apoptosis, and significantly improved RGC survival. NDUFS1 downregulation plays a critical role in glaucomatous RGC injury. Overexpression of NDUFS1 improves mitochondrial function, attenuates OS, and enhances cell survival. The study provides novel mechanistic insights into neuroprotection in glaucoma and suggests NDUFS1 as a potential therapeutic target.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110913"},"PeriodicalIF":2.7,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146164736","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":"Decreased corneal biomechanical stability and structural integrity in PPAR-α knockout mice","authors":"Chengfang Zhu ,&nbsp;Huan He ,&nbsp;Hongwei Yan ,&nbsp;Aolin Liu ,&nbsp;Minghui Liang ,&nbsp;Rongrong Zong ,&nbsp;Bin Liu ,&nbsp;Xiuxian Qin ,&nbsp;Juan Yang ,&nbsp;Zhirong Lin","doi":"10.1016/j.exer.2026.110911","DOIUrl":"10.1016/j.exer.2026.110911","url":null,"abstract":"<div><div>Recent evidence indicates that inflammatory cytokines and proteolytic enzymes play a vital role in the development of biomechanical failure in the cornea. Previous studies have shown that inflammatory cascades could be inhibited by peroxisome proliferator-activated receptor-α activation. This study seeks to investigate the biomechanical and structural features of the cornea in PPAR-α−/− mice and to assess alterations in inflammatory cytokines and enzymes. Adult PPAR-α^−/− mice and wild-type C57BL/6 mice (WT) were used in this study. The corneas were excised and evaluated by modulus of elasticity test, enzymatic tissue digestion assay, corneal fluorescein sodium staining, tear film break-up time (tBUT), anterior segment OCT, in vivo corneal confocal microscopy (IVCM), transmission electron microscopy (TEM), and quantitative real-time PCR (RT-PCR). Decreased tBUT and SIt values were observed, while no corneal lesions were observed in the PPAR-α^−/− mice. The corneal tangent modulus at fracture and resistance to enzymatic hydrolysis in PPAR-α^−/− mice were significantly decreased (<em>P</em> = 0.005 and <em>P</em> &lt; 0.001, respectively). Anterior segment OCT showed that the corneas of PPAR-α^−/− mice were significantly thinner than in the WT (<em>P</em> = 0.008). IVCM showed that the corneal nerve fibers of PPAR-α^−/− mice were slender, and the hypo-reflective folds of the stromal layer were more apparent, while the stromal fibers of the WT were thicker. TEM showed that the lamellar stromal fibers were interlaced and disorganized with decreased fiber density in PPAR-α^−/− mice compared with the WT. The expression of F-actin, lumican, laminin, TGF-β, TIMP-1, and TIMP-3 in the cornea of PPAR-α^−/− mice was also decreased, accompanied by an increase of TNF-α and MMP-9. In conclusion, the corneal biomechanical stability and microstructural integrity of PPAR-α^−/− mice were decreased, which might be associated with dysregulation of corneal structure-related components, inflammation-related factors, and proteases.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110911"},"PeriodicalIF":2.7,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146164709","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":"Integrated proteomic and nitrosylomic profiling suggests a role for S-nitrosylation in choroidal dysregulation during myopia pathogenesis","authors":"Yuhang Liu ,&nbsp;Xiaohang Chen ,&nbsp;Ji Kou ,&nbsp;Xiangyi Wen ,&nbsp;Longqian Liu","doi":"10.1016/j.exer.2026.110909","DOIUrl":"10.1016/j.exer.2026.110909","url":null,"abstract":"<div><h3>Background</h3><div>Myopia, a global health burden, is associated with choroidal dysfunction, but the role of post-translational modifications, specifically S-nitrosylation (SNO), in its pathogenesis remains unclear. This study aimed to characterize choroidal S-nitrosylation and proteomic changes in lens-induced myopia (LIM) to identify SNO-driven regulatory pathways.</div></div><div><h3>Methods</h3><div>Myopia was induced in guinea pigs by unilateral −10 D lens wear (LIM group), with contralateral eyes as normal controls (NC). Ocular changes were assessed by axial length (AL) and refractive error measurements. Choroidal thickness was evaluated via Hematoxylin and Eosin (H&amp;E) staining. Global S-nitrosylation changes were detected by the biotin-switch assay coupled with Western blotting. Integrated proteomic and S-nitrosylomic profiling of choroidal tissues was performed using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Bioinformatic analyses included functional enrichment analysis and integrative nine-quadrant analysis to identify proteins regulated primarily via S-nitrosylation independent of abundance changes.</div></div><div><h3>Results</h3><div>The LIM model induced significant axial elongation (normalized AL elongation: 0.40 ± 0.68 mm) and a myopic shift (−7.11 ± 1.22 D), accompanied by significant choroidal thinning (49.69 ± 8.67 μm in LIM vs. 70.96 ± 8.90 μm in NC, P = 0.00004). Total choroidal S-nitrosylated protein levels were significantly upregulated in LIM. Integrated dual-omics analysis identified 1293 proteins (corresponding to 1651 modification sites) with significant SNO changes without concomitant protein abundance alterations. Among these, 711 proteins (910 sites) showed upregulated S-nitrosylation in the LIM group. Functional enrichment analysis of these proteins implicated key pathways including Cytoskeleton in muscle cells, Synaptic vesicle cycle, and Ferroptosis. Critical candidates such as HSPG2, FN1, SPTBN1, NSF, and GPX4 were prioritized, suggesting their involvement in extracellular matrix integrity, neurovascular communication, and oxidative stress defense.</div></div><div><h3>Conclusion</h3><div>This study provides the first integrated map of choroidal proteome and S-nitrosylome in myopia, establishing S-nitrosylation as a pivotal post-translational regulatory layer. The data suggest that SNO-mediated dysregulation of cytoskeletal integrity, synaptic signaling, and ferroptosis pathways may contribute to choroidal thinning and dysfunction during myopia progression. These findings nominate specific SNO-modified proteins and their associated pathways as novel potential therapeutic targets for myopia intervention. Future work should focus on the functional validation of the identified SNO sites.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110909"},"PeriodicalIF":2.7,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146164704","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":"Effect of chemokine and chemokine-receptor gene polymorphisms on the development of diabetic retinopathy in the Turkish cohort","authors":"Ebru Alp ,&nbsp;Egemen Akgun ,&nbsp;Sibel Doguizi ,&nbsp;Fadime Mutlu Icduygu ,&nbsp;Mehmet Ali Sekeroglu ,&nbsp;Murat Atabey Ozer","doi":"10.1016/j.exer.2026.110912","DOIUrl":"10.1016/j.exer.2026.110912","url":null,"abstract":"<div><div>It is known that in many acute and chronic inflammatory diseases, chemokines are secreted into the environment and increase during the inflammation process. Inflammation is thought to be important in the pathogenesis of diabetic retinopathy (DR) and various cytokines and chemokines play a role. Accordingly, the aim of the present study is to determine the relationship between DR and chemokines and their receptor gene polymorphisms (CXCL12, CXCR4, CCL2, CCR2) in Turkish population. This study included 353 patients with type 2 diabetes mellitus (with and without retinopathy) and 204 controls. Genomic DNA was isolated from whole blood and genotype distribution of polymorphisms was determined by PCR-RFLP method. It was determined that the G allele of the CCL2 rs1024611 SNP could prevent the development of DR (1.42 fold) and PDR (proliferative diabetic retinopathy) (1.92 fold). Binary logistic regression analysis also showed that the TT genotype of CXCL12 rs1801157 SNP may have a protective effect (OR = 0.258) on the development of DR. In contrast, CXCR4/rs2228014 and CCR2/rs1799864 SNPs did not show a significant effect on DR in the Turkish population. Findings of the present study suggest that the CCL2 rs1024611 SNP may play a role in the etiology of DR and PDR, and the G allele has a protective effect in Turkish population. Furthermore, TT genotype of CXCL12 rs1801157 SNP may also provide protection against the development of DR. Large-scale studies including a large number of patients are recommended to confirm these results.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"266 ","pages":"Article 110912"},"PeriodicalIF":2.7,"publicationDate":"2026-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146156484","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":"The CD74-MIF axis contributes to acute uveitic injury by upregulating proinflammatory cytokine secretion in murine cytomegalovirus intracameral infection mouse models","authors":"Qilian Sheng ,&nbsp;Suqian Wu ,&nbsp;Kwan Yelin ,&nbsp;Yijia Yang ,&nbsp;Yue Ying ,&nbsp;Yanan Sun ,&nbsp;Yun Cheng ,&nbsp;Xiangmei Kong","doi":"10.1016/j.exer.2026.110907","DOIUrl":"10.1016/j.exer.2026.110907","url":null,"abstract":"<div><div>Murine cytomegalovirus (MCMV) intracameral infection successfully models clinical manifestations resembling CMV-positive Posner-Schlossman Syndrome (PSS). We observed distinct phenotypes in infected C57BL/6 and BALB/c mice: C57BL/6 exhibited severe intraocular inflammation with corneal edema and persistent elevated intraocular pressure (IOP), while BALB/c showed acute IOP spikes with mild uveitis. Single-cell sequencing revealed significant upregulation of CD74 in intraocular CD45⁺ immunocytes of C57BL/6 mice. CD74, a receptor for macrophage migration inhibitory factor (MIF), is a key regulator of inflammatory pathways. This study found that C57BL/6 with MCMV intracameral infection exhibited increased CD74⁺ cell counts systemically and intraocularly, alongside elevated intraocular and systemic levels of MIF and various inflammatory cytokines. In vitro, recombinant MIF enhanced cytokine secretion (including IL-6, IL-1β, CCL2, CCL5and CXCL1) in primary peripheral blood mononuclear cells (PBMCs), while CD74 blockade partially inhibited MIF-induced cytokine production. The CD74-MIF interaction is indispensable for cytokine secretion in downstream inflammatory pathways. These findings suggest that the CD74-MIF axis drives ocular inflammation and uveitic damage following MCMV infection in C57BL/6 mice, highlighting its potential as a therapeutic target for immunosuppression in acute uveitis.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"265 ","pages":"Article 110907"},"PeriodicalIF":2.7,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146141444","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":"Interactions of choroid and sclera in the myopia model of the chicken","authors":"Ute Mathis ,&nbsp;Gustav Christensen ,&nbsp;Marita Feldkaemper ,&nbsp;Falk Schroedl ,&nbsp;Alexandra Kaser-Eichberger ,&nbsp;Frank Schaeffel","doi":"10.1016/j.exer.2026.110904","DOIUrl":"10.1016/j.exer.2026.110904","url":null,"abstract":"<div><h3>Purpose</h3><div>Changes in choroidal thickness are currently used to predict future refractive error development but there is incomplete knowledge about the communication between choroid and sclera. We studied how choroidal thickness changes interact with scleral thickness changes and how the abundance of dopamine (DA)- and all-trans retinoic acid (atRA)-synthetizing choroidal cells varies when choroidal thickness is altered by drugs.</div></div><div><h3>Methods</h3><div>Changes in choroidal thickness were induced by a single intravitreal injection in the morning of the muscarinic antagonist atropine, the DA agonist apomorphine or the DA antagonist spiperone. Thickness of the choroid and the scleral layers was measured by spectral domain optical coherence tomography (SD-OCT). Immunocytochemistry was used to study the distribution of dopamine-synthetizing structures in the choroid and their colocalisation with retinaldehyde dehydrogenase 2 (RADLH2), the key synthetizing enzyme of atRA.</div></div><div><h3>Results</h3><div>(1) Both atropine and apomorphine increased choroidal thickness over the day while spiperone resulted in a decrease. (2) For apomorphine and spiperone, choroidal thickness changes were positively correlated with thickness changes in both the cartilaginous and fibrous layers of the sclera. With atropine, only the cartilaginous layer thickened. (3) DA was co-localized with RALDH2 in stromal cells in the choroid in a few cases but the numbers of double-stained cells increased massively after drug injections. (4) RALDH2-immunoreactivity (indicating atRA activity) increased, no matter whether the choroid and the sclera thickened or thinned.</div></div><div><h3>Conclusions</h3><div>Following drug injections, thickness changes of choroid and sclera were correlated and occurred without phase delay. Numbers of DA and RALDH2 co-expressing cells in the choroid increased. Choroidal dopaminergic cells that synthesize atRA appear to act as activators of scleral metabolic activity during both scleral growth stimulation and inhibition.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"265 ","pages":"Article 110904"},"PeriodicalIF":2.7,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131646","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}