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Background: Myopia is one of the most common eye diseases globally, and has become an increasingly serious health concern among adolescents. Understanding the factors contributing to the onset of myopia and the strategies to slow its progression is critical to reducing its prevalence. Main text: Animal models are key to understanding of the etiology of human diseases. Various experimental animal models have been developed to mimic human myopia, including chickens, rhesus monkeys, marmosets, mice, tree shrews, guinea pigs and zebrafish. Studies using these animal models have provided evidences and perspectives on the regulation of eye growth and refractive development. This review summarizes the characteristics of these models, the induction methods, common indicators of myopia in animal models, and recent findings on the pathogenic mechanism of myopia. Conclusions: Investigations using experimental animal models have provided valuable information and insights into the pathogenic mechanisms of human myopia and its treatment strategies.

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BACKGROUND: Myopia is one of the eye diseases that can damage the vision of young people. This study aimed to explore the protective role of miR-92b-3p against DNA damage and apoptosis in retinal tissues of negative lens-induced myopic (LIM) guinea pigs by targeting BTG2. METHODS: Biometric measurements of ocular parameters, flash electroretinogram (FERG), and retinal thickness (RT) were performed after miR-92b-3p intravitreal injection in LIM guinea pigs. The apoptotic rate was detected by Annexin V-FITC/PI double staining, and the change in mitochondrial membrane potential was measured by JC-1 staining. Retinal apoptosis and expression of p53, BTG2, and CDK2 were explored by TdT-mediated dUTP-biotin nick labeling (TUNEL) and immunofluorescence staining assays, respectively. BTG2 and its upstream and downstream molecules at gene and protein levels in retinal tissues were measured by real-time quantitative PCR (qPCR) and Western blotting. RESULTS: Compared with normal controls (NC), the ocular axial length of LIM guinea pig significantly increased, whereas refraction decreased. Meanwhile, dMax-a and -b wave amplitudes of ERG declined, retinal thickness was decreased, the number of apoptotic cells and apoptotic rate in LIM eyes was exaggerated, and the mitochondrial membrane potential significantly decreased. In addition, results of qPCR and Western blot assays showed that the expression levels of p53, BTG2, CDK2, and BAX in LIM guinea pigs were higher than the levels of the NC group, whereas the BCL-2 expression level was decreased. By contrast, the miR-92b-3p intravitreal injection in LIM guinea pigs could significantly inhibit axial elongation, alleviate DNA damage and apoptosis, and thus protect guinea pigs against myopia. CONCLUSION: In conclusion, p53 and BTG2 were activated in the retinal tissue of myopic guinea pigs, and the activated BTG2 could elevate the expression of CDK2 and BAX, and attenuate the expression of BCL-2, which in turn promote apoptosis and eventually lead to retinal thinning and impaired visual function in myopic guinea pigs. The miR-92b-3p intravitreal injection can attenuate the elongation of ocular length and retinal thickness, and inhibit the CDK2, BAX, and p53 expression by targeting BTG2, thereby ameliorating DNA damage and apoptosis in LIM guinea pigs and protecting ocular tissues.

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BACKGROUND: To investigate the relationship between body weight and Axial length in guinea pigs. METHODS: Forty pigmented guinea pigs were randomly divided into two groups, namely control group and negative lens-induced myopization (LIM) group. After measuring the baseline axial length and body weight (BW), guinea pigs of LIM group received bilateral negative lens-induced myopization using - 10.0 diopters lenses. One week later, the lenses were removed and biometric and ophthalmoscopic examinations were repeated. RESULTS: Two groups of guinea pigs showed no statistical difference in initial body weight and eye axis length. Compared to the control group, the lens-induced group had a lower weight (P = 0.02) and a longer axial length (P < 0.01) at the end of study Neither at baseline nor at week 1 did AL correlate with BW in both groups (Control Baseline: r = 0.306, P = 0.19; Control Week1: r = 0.333, P = 0.15; LIM Baseline: r=-0.142, P = 0.55; LIM Week 1: r = 0.189, P = 0.42). Lens-induction had a significant effect on axial elongation (P < 0.01) while body weight had no impact on such aspect (P > 0.05). CONCLUSION: In guinea pigs of the same age, axial length was not correlated with body weight. Also, baseline body weight had no impact on natural axial length growth or lens-induced myopia. Lens-induction caused a significant reduction in body weight gain.

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Purpose: Bright light conditions are supposed to curb eye growth in animals with experimental myopia. Here we investigated the effects of temporal bright light at very low frequencies exposures on lens-induced myopia (LIM) progression. Methods: Myopia was induced by application of -6.00 D lenses over the right eye of guinea pigs. They were randomly divided into four groups based on exposure to different lighting conditions: constant low illumination (CLI; 300 lux), constant high illumination (CHI; 8,000 lux), very low frequency light (vLFL; 300/8,000 lux, 10 min/c), and low frequency light (LFL; 300/8,000 lux, 20 s/c). Refraction and ocular dimensions were measured per week. Changes in ocular dimensions and refractions were analyzed by paired t-tests, and differences among the groups were analyzed by one-way ANOVA. Results: Significant myopic shifts in refractive error were induced in lens-treated eyes compared with contralateral eyes in all groups after 3 weeks (all P < 0.05). Both CHI and LFL conditions exhibited a significantly less refractive shift of LIM eyes than CLI and vLFL conditions (P < 0.05). However, only LFL conditions showed significantly less overall myopic shift and axial elongation than CLI and vLFL conditions (both P < 0.05). The decrease in refractive error of both eyes correlated significantly with axial elongation in all groups (P < 0.001), except contralateral eyes in the CHI group (P = 0.231). LFL condition significantly slacked lens thickening in the contralateral eyes. Conclusions: Temporal bright light at low temporal frequency (0.05 Hz) appears to effectively inhibit LIM progression. Further research is needed to determine the safety and the potential mechanism of temporal bright light in myopic progression.

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OBJECTIVE: This study aimed to investigate the regulatory role of the PI3K/AKT/ERK signaling pathway in retinal fibrosis in -6.0 diopter (D) lens-induced myopic (LIM) guinea pigs. METHODS: Biological measurements of eye tissues were performed on guinea pigs to obtain their refraction, axial length, retinal thickness, physiological function, and fundus retinal status. In addition, Masson staining and immunohistochemical (IHC) assay were further done to explore the changes in retinal morphology after myopic induction. Meanwhile, hydroxyproline (HYP) content was measured to evaluate the degree of retinal fibrosis. Moreover, the levels of the PI3K/AKT/ERK signaling pathway and fibrosis-related molecules in retinal tissues including matrix metalloproteinase 2(MMP2), collagen type I (Collagen I), and α-smooth muscle actin (α-SMA) were detected by real-time quantitative PCR (qPCR) and Western blot. RESULTS: The LIM guinea pigs showed a significant myopic shift in refractive error and an increase in axial length compared with those of the normal control (NC) group. Masson staining, hydroxyproline content determination, and IHC showed an increase in retinal fibrosis. After myopic induction, qPCR and western blot analyses showed that phosphatidylinositol-3-kinase catalytic subunit α (PIK3CA), protein kinase B (AKT), extracellular regulated protein kinase 1/2 (ERK1/2), MMP2, Collagen I, and α-SMA were consistently elevated in the LIM group than those in the NC group. CONCLUSION: The PI3K/AKT/ERK signaling pathway was activated in the retinal tissues of myopic guinea pigs, which exaggerated fibrotic lesions and reduced retinal thickness, ultimately leading to retinal physiological dysfunctions in myopic guinea pigs.

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Myopia is one of the most common eye diseases in children and adolescents worldwide. Currently, there is no effective treatment in clinical practice. Ocular tissue fibrosis is involved in the development of myopia and this study aimed to investigate the effect of miR-138-5p on choroidal fibrosis in myopic guinea pigs via regulating the HIF-1α signaling pathway. First, guinea pigs were randomly divided into a normal control (NC) group, a lens-induced myopia (LIM) group, a LIM + miR-138-5p-carried Lentivirus treatment (LV) group, and a LIM + miR-138-5p-Vector treatment (VECTOR) group. All animals were induced experimental myopia with a -6.0 diopter lens except those in the NC group. Meanwhile, animals in the LV group were supplemented with 5 µl of miR-138-5p-carried Lentivirus, while those in the VECTOR group were only supplemented with the same volume of miR-138-5p-Vector. After myopia induction for 2 and 4 weeks, the refractive status and other ocular parameters of the guinea pigs were measured. Further, the expression of hypoxia-inducible factor (HIF)-1α, transforming growth factor (TGF)-ß, collagen I, hydroxyproline (HYP), interleukin 1 beta (IL-1ß), tumor necrosis factor alpha (TNF-α), and a-smooth muscle actin (α-SMA) in choroidal tissues was investigated. Results showed that the refraction and axial length of the experimental myopic guinea pigs increased, and choroid fibrosis aggravated after experimental myopic induction. miR-138-5p can efficiently decrease the refraction and ocular length, and ameliorate the choroidal fibrosis of the experimental myopic guinea pigs via downregulating the fibrosis-related TGF-ß1, collagen I, HYP, IL-1ß, TNF-α, and α-SMA expression through inhibiting the HIF-1α signaling pathway. Our results provide new insight into controlling myopic development using microRNAs in clinical practice.

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Animal models have been indispensable in shaping the understanding of myopia mechanisms, with form-deprivation myopia (FDM) and lens-induced myopia (LIM) being the most utilized. Similar pathological outcomes suggest that these two models are under the control of shared mechanisms. miRNAs play an important role in pathological development. Herein, based on two miRNA datasets (GSE131831 and GSE84220), we aimed to reveal the general miRNA changes involved in myopia development. After a comparison of the differentially expressed miRNAs, miR-671-5p was identified as the common downregulated miRNA in the retina. miR-671-5p is highly conserved and related to 40.78% of the target genes of all downregulated miRNAs. Moreover, 584 target genes of miR-671-5p are related to myopia, from which we further identified 8 hub genes. Pathway analysis showed that these hub genes are enriched in visual learning and extra-nuclear estrogen signaling. Furthermore, two of the hub genes are also targeted by atropine, which strongly supports a key role of miR-671-5p in myopic development. Finally, Tead1 was identified as a possible upstream regulator of miR-671-5p in myopia development. Overall, our study identified the general regulatory role of miR-671-5p in myopia as well as its upstream and downstream mechanisms and provided novel treatment targets, which might inspire future studies.

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PURPOSE: Apart from genetic factors, recent animal studies on myopia have focused on localised mechanisms. In this study, we aimed to examine the contralateral effects of monocular experimental myopia and recovery, which cannot be explained by a mere local mechanism. METHODS: One eye of 3-week-old C57BL/6 male mice was fitted with a -30 dioptre (D) lens. The mice were distributed into two groups based on different conditions in the contralateral eye: either no lens (NLC) (n = 10) or a Plano lens on the contralateral eye (PLC) group (n = 6). Mice receiving no treatment on either eye were set as a control group (n = 6). Lenses were removed after 3 weeks of myopia induction. All mice were allowed to recover for 1 week in the same environment. Refractive status, axial length (AL) and choroidal thickness were measured before myopia induction, after 1 and 3 weeks of lens wear and after 1 week of recovery. RESULTS: One week after removing the lenses, complete recovery was observed in the eyes that wore the -30 D lenses. In both the PLC and NLC groups, the refractive status showed a myopic shift after lens removal. Additionally, the choroid was significantly thinned in these eyes. The -30 D wearing eye showed a significant increase in AL after 3 weeks of lens wear. While the AL of the -30 D wearing eye ceased to grow after the lens was removed, the AL in the PLC and NLC contralateral eyes increased, and the binocular ALs gradually converged. CONCLUSIONS: Recovery of lens-induced myopia was observed in mouse models. In the fellow eyes, the effects, including thinning of the choroid and changes in refractive status, were triggered by contralateral visual cues.

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AIM: To examine the effects of salidroside on choroidal thickness, hypoxia-inducible factor-1α(HIF-1α), dopamine(DA)and its D1 receptor expression in guinea pigs with lens-induced myopia(LIM).METHODS: A total of 18 two-week-old guinea pigs were randomly divided into the normal control(NC)group, the LIM group, and the LIM + salidroside(LIM+SA)group, with 6 guinea pigs in each group. The guinea pigs in the NC group were fed normally and intragastrically administered with 2 mL/d saline; those in the LIM group wore a -5D lens in front of their right eyes to establish a myopia model, then they were intragastrically administered with 2 mL/d saline. Finally, those in the LIM+SA group wore glasses along with intragastric administration of 2 mL/d salidroside at a dose of 100 mg/kg. The refraction, axial length, and choroidal thickness of guinea pigs in each group were measured 4wk following the establishment of the model. In addition, the relative mRNA expression and protein content of HIF-1α in the choroid and retina of guinea pigs in each group were detected by real-time quantitative PCR(qPCR)and immunohistochemistry(IHC). Finally, the DA concentration and its D1 receptor expression were detected by enzyme-linked immunosorbent assay(ELISA)and Western blot.RESULTS: At 4wk after model establishment, guinea pigs of LIM group and LIM+SA group exhibited increased negative refraction of the right eye, prolonged axial length, and decreased choroidal thickness compared to the NC group. The relative mRNA expression and protein content of HIF-1α in the choroid and retina of the guinea pigs increased. The concentration of DA and the expression of its D1 receptor both decreased. Moreover, compared to the LIM group, the diopter of the right eye of guinea pigs in LIM+SA group significantly reduced, the axial length was shorter, the thickness of choroid increased, the relative mRNA expression and protein content of HIF-1α in the choroid and retina decreased and the concentration of DA and the expression of its D1 receptor both increased.CONCLUSION: Salidroside can delay myopia progression in myopic guinea pigs by affecting choroidal thickness and the expression of HIF-1α, DA and its D1 receptor.

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Objective:To observe the effects of blue light intervention on the development of optical defocus-induced myopia in guinea pigs and investigate its underlying mechanisms.Methods:Forty-eight normal-grade two-week-old tricolor guinea pigs were randomly divided into a blue light group and a white light group, with 24 animals in each group.The right eye of guinea pigs was fitted with a -5.00 D lens to establish an optical defocus model as the experimental eye, while the left eye served as the control without any covering.Before the experiment and after 8-week intervention, the refractive power of guinea pigs was measured by streak retinoscopy.The anterior chamber depth, lens thickness, and axial length were measured by A-scan ultrasonography.Corneal curvature radius was determined using a keratometer.After 8-week intervention, the guinea pigs were euthanized through overanesthesia, and the right eyeballs were enucleated and the retinas were isolated.The density of S and M cone cells of the guinea pig retinal sections were observed via immunofluorescence staining.The expression of retinal retinoic acid was assessed by high-performance liquid chromatography.The expressions of retinoic acid receptor (RAR-β) in the retina and matrix metalloproteinase-2 (MMP-2), tissue inhibitor of metalloproteinase-2 (TIMP-2), and type Ⅰ collagen in the sclera were detected by real-time fluorescence quantitative PCR.Changes in scleral thickness were observed through hematoxylin-eosin staining.The use and care of the animals complied with Regulations for the Administration of Affair Concerning Experimental Animals by State Science and Technology Commission.The study protocol was approved by the Ethics Committee of Eye and ENT Hospital of Fudan University (No.2022ETKLD10032).Results:After 8 weeks of intervention, guinea pigs in the blue light group showed (0.63±0.12)D of relative hyperopia and a deceleration of axial elongation by (0.08±0.00)mm compared with the white light group in the right eye.In the left eye, guinea pigs in the blue light group showed (0.42±0.09)D of relative hyperopia and a deceleration of axial elongation by (0.08±0.00)mm compared with the white light group.The guinea pigs in blue light group showed (1.52±0.09)D of myopia in the right eye compared with the left eye, with an increase in axial elongation of (0.06±0.00)mm.The guinea pigs in white light group showed (1.66±0.07)D of myopia in the right eye compared with the left eye, with an increase in axial elongation of (0.13±0.00)mm, and the differences were statistically significant (all at P<0.05). The density of M cone cells was lower and density of S cone cells was higher in the blue light group in the dorsal and ventral sides of the retinal sections compared with the white light group, showing statistically significant differences ( t=32.33, 52.23, 42.09, 25.02; all at P<0.05). The deceleration of myopia progression in the blue light group was strongly positively correlated with the increase in S cone cell density on the ventral side ( r=0.95, P<0.01). The expression levels of retinoic acid, RAR-β, and MMP-2 were decreased, and expression levels of TIMP-2 and type Ⅰ collagen were increased in blue light group compared with the white light group, showing statistically significant differences ( t=18.73, 7.45, 3.72, 6.19, 9.03; all at P<0.05). The scleral thickness in the blue light group was (125.0±7.8)μm, which was significantly thicker than (102.0±6.3)μm in the white light group ( t=26.93, P<0.05). Conclusions:Blue light intervention can inhibit the progression of defocus-induced myopia in guinea pigs.Refractive power changes in guinea pigs may be influenced by alterations in retinal cone cell density, retinoic acid expression, and scleral collagen expression.

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PURPOSE: To report the surgical outcome of early lens aspiration, posterior chamber intraocular lens (PC IOL), and capsular tension ring (CTR) in a case series of microspherophakia (MSP) and secondary glaucoma. METHODS: Case series of 18 eyes of MSP cases presented with lenticular myopia and secondary glaucoma that underwent early lens aspiration, PC IOL and CTR by one ophthalmologist. Baseline, long-term postoperative outcomes and complications were documented. RESULTS: All cases underwent successful surgery with lens aspiration PC IOL implantation and CTR insertion without intraoperative complications. One of the 18 cases was a delayed referral which had broad anterior synechiae and following lens aspiration developed corneal decompensation. In one eye, CTR implantation was not possible hence, lens aspiration with scleral fixation (SF) of 3 piece IOL was performed (excluded from the analysis). Overall there was an improvement in visual acuity (from 0.3 ± 0.1 to 0.2 ± 0.2 LogMar, P = 0.006), intraocular pressure (IOP), and most notably, deepening of the anterior chamber. Some cases required subsequent glaucoma surgery to control IOP. After a long duration of follow-up, all cases had stable capsular lens complex and no capsular phimosis. CONCLUSION: Early Lens aspiration with CTR and PCIOL alone in MSP with lens subluxation has a significant impact on the patient's quality of vision, deepening the anterior chamber and preventing complications or poor outcomes. In addition, good capsular-lens complex stability and absence of capsular phimosis or phacodonesis on long-term follow-up were obtained.

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Topiramate (TPM) is a sulfonamide drug with multiple modes of action. It inhibits carbonic anhydrase, blocks sodium channels, enhances potassium channels, and stimulates postsynaptic gamma-aminobutyric acid (GABA) receptors. Pharmacists Joe Gardocki and Bruce Maryanoff synthesized TPM for the first time in 1979. The FDA did not approve it for medical use in the US until 1996. Around 2004, it was authorized for the prevention of migraine headaches. TPM, like any medication, has several side effects. Common aftermaths include weight loss, diarrhea, dizziness, sleepiness, fatigue, and coordination issues. Some people may experience mental health issues like memory problems, confusion, and speech or language difficulties. The most well-known ocular side effects of TPM are choroidal effusion syndrome, angle-closure glaucoma, and myopic shift. Aside from these, other ophthalmic adverse effects may arise in some people, including retinal problems, uveitis, visual field defects, myokymia, and neuro-ophthalmology complications. If such complications are not identified and treated promptly, they can be severe and vision-threatening, potentially leading to permanent blindness. TPM's application as a standalone and adjunctive therapy has increased over time. In 2019, more than 10 million prescriptions of TPM were issued. Due to its extensive use, medical professionals and patients must be aware of its potential repercussions, especially ophthalmic issues. The current review paper likewise makes a step in this direction. This article's primary purpose is to educate readers by providing a comprehensive assessment of the research on TPM's ocular side effects. All the information has been collected via a thorough search of the Google Search Engine and PubMed.

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Marfan syndrome is an orphan disease that is caused by a mutation in the FBN1 gene located on chromosome 15 (15q21.1) and is usually inherited in an autosomal dominant manner. The article reviews the results of studies concerning the potential ocular manifestations of Marfan syndrome.

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Although reduced ambient lighting (~50 lx) does not increase the degree of form-deprivation myopia (FDM) in chickens or infant monkeys, it does reduce the probability that monkeys will recover from FDM and that the normal age-dependent reduction in hyperopia will occur in monkeys reared with unrestricted vision. These findings suggest that low ambient lighting levels affect the regulatory mechanism responsible for emmetropization. To study this issue, infant rhesus monkeys (age ~ 24 days) were reared under dim light (55 ± 9 lx) with monocular -3D (dim-light lens-induced myopia, DL-LIM, n = 8) or +3D spectacle lenses (dim-light lens-induced hyperopia, DL-LIH, n = 7) until approximately 150 days of age. Refractive errors, ocular parameters and sub-foveal choroidal thickness were measured periodically and compared with normal-light-reared, lens-control monkeys (NL-LIM, n = 16; NL-LIH, n = 7). Dim light rearing significantly attenuated the degree of compensatory anisometropias in both the DL-LIM (-0.63 ± 0.77D vs. -2.11 ± 1.10D in NL-LIM) and DL-LIH treatment groups (-0.18 ± 1.93D vs. +1.71 ± 0.39D in NL-LIH). These effects came about because the treated and fellow control eyes had a lower probability of responding appropriately to the eye's effective refractive state. Vision-induced interocular differences in choroidal thickness were only observed in monkeys that exhibited compensating refractive changes, suggesting that failures in detecting the relative magnitude of optical errors underlay the abnormal refractive responses. Our findings suggest that low ambient lighting levels reduce the efficacy of the vision-dependent mechanisms that regulate refractive development.

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INTRODUCTION: This study aimed to determine the role of the choroid in lens-induced myopia (LIM) in guinea pigs. METHODS: Guinea pigs were randomly divided into two groups: a normal control (NC) group and a LIM group. Refraction and axial length (AL) were measured by streak retinoscopy and A-scan ultrasonography. The choroidal thickness (ChT), vessel density of the choriocapillaris (VDCC) and vessel density of the choroidal layer (VDCL) were assessed by Spectral-domain Optical Coherence Tomography Angiography (SD-OCT). In addition, the choroidal expression of nitric oxide synthase (NOS) enzymes at the mRNA and protein levels was analyzed by real-time fluorescence quantitative PCR, enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry. RESULTS: In the LIM group, refraction and AL were increased significantly compared with those in the NC group at 2 weeks (refraction: LIM vs. NC, -4.23 ± 0.43 D vs. 2.20 ± 0.48 D; AL: LIM vs. NC, 8.36 ± 0.05 mm vs. 8.22 ± 0.03 mm) and 4 weeks (refraction: LIM vs. NC, -5.88 ± 0.49 D vs. 1.63 ± 0.41 D; AL: 8.57 ± 0.06 mm vs. 8.40 ± 0.04 mm). The ChT and VDCC were decreased significantly compared with those in the NC group at 2 weeks (ChT: LIM vs. NC, 60.92 ± 8.15 µm vs. 79.11 ± 7.47 µm; VDCC: LIM vs. NC, 23.43 ± 3.85% vs. 28.74 ± 4.11%) and 4 weeks (ChT: LIM vs. NC, 48.43 ± 6.85 µm vs. 76.38 ± 7.84 µm; VDCC: LIM vs. NC, 21.29 ± 2.17% vs. 27.64 ± 2.91%). The VDCL was also decreased compared with that in the NC group at 2 weeks and 4 weeks (NC vs. LIM, 24.87 ± 5.16% vs. 22.45 ± 3.26%; 23.37 ± 5.85% vs. 21.39 ± 2.62%; all P > 0.05). Moreover, the ChT was positively correlated with the VDCC and VDCL. The mRNA and protein expression of NOS enzymes (eNOS and nNOS) was increased. CONCLUSIONS: During the development of myopia, the ChT, VDCC and VDCL were decreased, while NOS expression in the choroid was increased. The expression of NOS was negatively correlated with the ChT, VDCC and VDCL. NO may play an important role in regulating the choroid during myopia development.

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@#AIM:To observe the changes of the vessel density of choriocapillaris in lens-induced myopia in guinea pigs, and to explore choroidal endothelin-1(ET-1), endothelin receptor A(ETAR)and receptor B(ETBR)expression changes and the effect of electroacupuncture. <p>METHODS: Fifty-four guinea pigs were randomly divided into normal control(NC), lens-induced myopia(LIM)and LIM+electroacupuncture(LIM+EA). The NC group was fed normally without intervention and the right eye in LIM group and LIM+EA group was coverd with a -6.00D lens to establish a myopia model. At 2 and 4wk, the refraction, axial length and the vessel density of choriocapillaris in groups were measured. The expression and protein content of ET-1, ETAR and ETBR mRNA in groups were detected by the real-time fluorescent quantitative PCR(quantitative polymerase chain reaction, q-PCR), enzyme-linked immunosorbent assay(ELISA)and immunohistochemistry. <p>RESULTS: At 2 and 4wk, compared with the the NC group, refraction and axial length in LIM group and LIM+EA group had significantly increased(all <i>P</i><0.001). Compared with the LIM group, the refraction and axial length in LIM+EA group were decreased(all <i>P</i><0.05). At 2 and 4wk, compared with the NC group,the vessel density of choriocapillaris was decreased(<i>P</i><0.001)and the ET-1, ETAR and ETBR mRNA and protein levels in choroid were increased(all <i>P</i><0.05)in LIM group. At 2 and 4wk, compared with the LIM group,the vessel density of choriocapillaris was decreased(<i>P</i><0.01)and the ET-1, ETAR and ETBR mRNA and protein levels in choroid were increased in LIM+EA group.<p>CONCLUSION:In LIM guinea pigs, the choroidal blood flow decreased with the increased of refraction and axial length, which may affect ET-1 and its receptors through vascular shear force during the development of myopia. At the same time, electroacupuncture can improve choroidal blood flow through neuromodulation and affects the vascular shear stress to down-regulate the content of ET-1 and its receptor to delay the development of myopia.

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Myopia is a main cause of preventable or treatable visual impairment, it has become a major public health issue due to its increasingly high prevalence worldwide. Currently, it is confirmed that the development of myopia is associated with the disorders of accommodation. As a dominant factor for accommodation, ciliary muscle contraction/relaxation can regulate the physiological state of the lens and play a crucial role in the development of myopia. To investigate the relationship between myopia and ciliary muscle, the guinea pigs were randomly divided into a normal control (NC) group and a negative lens-induced myopia (LIM) group, and the animals in each group were further randomly assigned into 2-week (n = 18) and 4-week (n = 21) subgroups in accordance with the duration of myopic induction of 2 and 4 weeks, respectively. In the present study, right eyes of the animals in LIM group were covered with -6.0 D lenses to induce myopia. Next, we performed the haematoxylin and eosin (H&E) staining to observe the pathological change of ciliary muscle, determined the contents of adenosine triphosphate (ATP) and lactate acid (LA), and measured the Na+/K+-ATPase expression and activity in ciliary muscles in both NC and LIM groups. Moreover, we also analyzed the potassium ion (K+) flux in ciliary muscles from 4-week NC and LIM guinea pigs. As a result, we found that the arrangements of ciliary muscles in LIM guinea pigs were broken, dissolved or disorganized; the content of ATP decreased, whereas the content of LA increased in ciliary muscles from LIM guinea pigs. Monitoring of K+ flux in ciliary muscles from LIM guinea pigs demonstrated myopia-triggered K+ influx. Moreover, we also noted a decreased expression of Na+/K+-ATPase (Atp1a1) at both mRNA and protein levels and reduced activity in ciliary muscles from LIM guinea pigs. Overall, our results will facilitate the understanding of the mechanism associated with inhibitory Na+/K+-ATPase in lens-induced myopia and which consequently lead to the disorder of microenvironment within ciliary muscles from LIM guinea pigs, paving the way for a promising adjuvant approach in treating myopia in clinical practice.

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BACKGROUND: Myopia is one of the most common vision defects worldwide. microRNAs can regulate the target gene expression, influencing the development of diseases. RESULTS: To investigate the alterations of microRNA profiling in negative lens-induced myopia (NLIM) guinea pigs and to explore the regulatory role of microRNAs in the occurrence and the development of myopia, we first established the NLIM guinea pig model after induction for 2 weeks. Further, we isolated sclera to purify total messenger RNA (mRNA) in both NLIM and NLIM fellow sclera. Using next generation sequencing technique and bioinformatics analysis, we identified the differentially expressed microRNAs in NLIM guinea pigs, performed the bioinformatics annotation for the differentially expressed microRNAs, and validated the expression of differentially expressed microRNAs. As a result, we successfully established an NLIM model in guinea pigs, identified 27 differentially expressed microRNAs in NLIM guinea pig sclera, including 10 upregulated and 17 downregulated microRNAs. The KEGG annotation showed the main signaling pathways were closely associated with PPAR signaling, pyruvate and propanoate metabolisms, and TGF-beta signaling pathways. CONCLUSIONS: Our findings indicate that the development of myopia is mainly involved in the disorder of metabolic processes in NLIM guinea pigs. The PPAR signaling, pyruvate and propanoate metabolism pathways may play roles in the development of myopia.

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To identify tissues and molecules involved in refractive myopic shift and axial length elongation in a murine lens-induced myopia model, we performed a comprehensive analysis of microRNA (miRNA) expression. Three weeks after negative 30 diopter lens fixation on three-week-old C57BL/6J mice, total RNA was extracted from individual ocular components including cornea, iris, lens, retina, retinal pigment epithelium (RPE)/choroid, and sclera tissue. The miRNA expression analysis was pooled from three samples and carried out using Agilent Mouse miRNA Microarray (8 × 60 K) miRBase21.0. The expression ratio was calculated, and differentially expressed miRNAs were extracted, using GeneSpring GX 14.5. Myopic induction showed a significant myopic refractive change, axial elongation, and choroidal thinning. Through the comprehensive miRNA analysis, several upregulated miRNAs (56 in cornea tissue, 13 in iris tissue, 6 in lens tissue, 0 in retina tissue, 29 in RPE/choroid tissue, and 30 in sclera tissue) and downregulated miRNAs (7 in cornea tissue, 28 in iris tissue, 17 in lens tissue, 9 in retina tissue, 7 in RPE/choroid tissue, and 40 in sclera tissue) were observed. Overlapping expression changes in miRNAs were also found in different ocular components. Some of this miRNA dysregulation may be functionally involved in refractive myopia shift and axial length elongation.

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PURPOSE: Several case reports of transient drug-induced myopia have been reported, mainly due to sulfa drugs. We present a case of a sudden and significant increase in myopia associated with initiation of Sulfasalazine for long-standing ulcerative colitis in an adult Caucasian female. CASE REPORT: Our patient presented to the emergency room with acute bilateral visual loss. Ocular examination was normal, except for myopia of -4 Diopters (D) in both eyes (BE). The patient was advised to stop the medication, and her vision improved within 4 days to best corrected visual acuity (BCVA) of 6/7.5 with a refractive correction of -0.75 D in her right eye (RE) and BCVA of 6/6 with a refractive correction of -0.50 D in her left eye (LE). CONCLUSION: To the best of our knowledge, this is the second reported case of transient Sulfasalazine-induced myopia.