Background: To evaluate early optical quality outcomes after small-incision lenticule extraction (SMILE) surgery for correcting high myopic astigmatism. Methods: This retrospective study enrolled 55 eyes from 37 patients who had preoperative myopic astigmatism of ≥2.00 diopters (D) who had been treated with SMILE surgery. Preoperatively, the mean cylinder was − 2.41 ± 0.54 D (range, − 2.00 D to − 4.50 D). The preoperative and postoperative visual outcomes, refraction, and higher-order aberration (HOA) at 1 and 3 months were compared. Refractive astigmatism changes were analyzed by the Alpins vector method. Results: Three months after SMILE surgery, the average cylinder was − 0.14 ± 0.31 D, and the average astigmatism vector was − 0.09 D × 6.34°. The angle of error (AofE) was limited to within ±10°, and the magnitude of error was limited to within ±1.0 D in all patients. The correction index (CI) was 0.98 ± 0.07, the index of success (IOS) was 0.08 ± 0.13, and the flattening index (FI) was 0.97 ± 0.07. Significant positive correlations were found between IOS and |AofE| (P = 0.000); negative correlations were found between FI and |AofE| (P = 0.000). The postoperative total HOA, spherical aberration, vertical coma aberration, and trefoil 30° were increased significantly compared with preoperative measurements, and the increase in HOA was closely related to preoperative astigmatism (P < 0.05). Conclusions: SMILE has preferable outcomes for correcting high myopic astigmatism. Axis rotation during the surgery might influence the undercorrection of astigmatism. The increase of HOA after surgery is related to preoperative astigmatism.

Background: Despite current intervention measures/therapies are able to ameliorate neuronal death following retinal injuries/diseases, the recovery of visual function remains unsatisfactory. Previous studies revealed that the retinal synapse and neurite changed during the early stage after retinopathy, which was considered to be detrimental to visual signal transmission. However, the specific profiles and the mechanisms underlying retinal neurite and synaptic alteration after retinal pathologies remain poorly understood. Methods: Here, we revealed the spatiotemporal pattern of neurite and synaptic alteration following retinal pathologies using a rat model of acute RI/R induced by high intraocular pressure (HIOP) with Western blotting, Immunofluorescence, and electron microscopy. We further explored the potential role of activated astrocytes and their derived thrombospondin 2 (TSP2) in RI/R induced retinal neurite and synaptic alteration and visual dysfunction through viral transduction and drug injection. Results: We found a defasciculation of RGC axons, a compensatory increase of presynaptic proteins (synaptophysin and synapsin 1) and synaptic vesicles between bipolar cells and ganglion cells in the inner plexiform layer (IPL), and the degenerated visual function preceded the neuronal death in rat retinae. These events were accompanied by the activation of astrocytes. Furthermore, we showed that suppressing the activation of astrocytes (intravitreal injection of fluorocitric acid, FC), TSP2 knockdown (TSP2 shRNA-AAV transduction), and competitively inhibiting the binding of TSP2 and α2δ1 (intraperitoneal injection of gabapentin, GBP) effectively alleviated the retinal synaptic and neurite alteration and the visual dysfunction following RI/R injury. Conclusions: (1) At the early stage following RI/R injury, the rat retinae develop a degeneration of ganglion cell axons and the resulting compensatory synaptic remodeling between bipolar cells and ganglion cells in IPL. These changes occur earlier than the massive loss of neurons in the ganglion cell layer (GCL). (2) Activated astrocytes may secret TSP2, which bind to α2δ1, to mediate the degeneration of rat retinal ganglion cell axons, compensatory synaptic remodeling in IPL, and visual dysfunction following RI/R injury.

The maintenance of visual function not only requires the normal structure and function of neurons but also depends on the effective signal propagation of synapses in visual pathways. Synapses emerge alterations of plasticity in the early stages of neuronal damage and affect signal transmission, which leads to transneuronal degeneration. In the present study, rat model of acute retinal ischemia/reperfusion (RI/R) was established to observe the morphological changes of neuronal soma and synapses in the inner plexiform layer (IPL), outer plexiform layer (OPL), and dorsal lateral geniculate nucleus (dLGN) after retinal injury. We found transneuronal degeneration in the visual pathways following RI/R concretely presented as edema and mitochondrial hyperplasia of neuronal soma in retina, demyelination, and heterotypic protein clusters of axons in LGN. Meanwhile, small immature synapses formed, and there are asynchronous changes between pre- and postsynaptic components in synapses. This evidence demonstrated that transneuronal degeneration exists in RI/R injury, which may be one of the key reasons for the progressive deterioration of visual function after the injury is removed.

Background. Myopia is a chronic ocular disease, emerging as the most common type of refractive error. This study intends to preliminarily explore the roles of protein S‐nitrosylation of nitric oxide (NO) in the regulation of myopia by detecting the expression of neuronal nitric oxide synthase (nNOS) and downstream S‐nitrosylation, using the animal model of lens‐induced myopia (LIM) in mice. Methods. The 3‐week‐old C57BL/6 J mice were divided into three groups: group I, lens‐induced 0‐week group (take eyeballs at the age of 3 weeks); group II, self‐control eyes of experimental group (take eyeballs at the age of 7 weeks); and group III, lens‐induced 4‐week group (take eyeballs at the age of 7 weeks). The diopter and axial length of each group were measured by streak retinoscopes and optical coherence tomography (OCT) before and after model establishment. The protein expressions and locations of nNOS and S‐nitrosylated proteins (PSNOs) were measured by western blot and immunofluorescence staining. Site‐specific proteomic for protein S‐nitrolysation was used to detect the existence and location of S‐nitrosylation proteins in the retina of myopic and nonmyopic mice. The Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and motif enrichment analyses were performed. The differential sites were analyzed by GO, KEGG, and motif. Irreversible biotinylation procedure combined with protein purification and western blot was used to detect the protein expression of α‐enolase (ENO1), a key player in the hypoxia‐related signal pathway. Results. The expressions of nNOS and PSNOs were significantly lower in the retina of experimental eyes than that in self‐control eyes and 3‐week‐old baseline group. A total of 595 S‐nitrosylated proteins, 709 S‐nitrosylated peptides, and 708 S‐nitrosylated sites were identified by site‐specific S‐nitrolysation proteomics in the retina of myopic and control eyes. A total of 19 differentiation loci were screened, of which 13 sites were downregulated and 6 sites were upregulated in experimental eyes compared with the self‐control group. Specifically, the expression of SNO‐ENO1 was significantly lower in the retina of experimental eyes than that in self‐control eyes and 3‐week‐old baseline group. Conclusion. LIM induces the decrease of nNOS and PSNO protein levels in the retina of myopic mice. NO‐mediated nonclassical protein S‐nitrosylation modification may play an important role in the regulation of lens‐induced myopia. ENO1 may be a key factor in the regulation of S‐nitrosylation modification of myopia.

Purpose. To investigate whether retinal neuroinflammatory response was affected by aging in a rat model of acute glaucoma. Methods. Young adult and aged rats were randomly assigned into normal control, 45mmHg, 60mmHg, and 90mmHg groups. Intraocular pressure (IOP) of rats was acutely elevated to 45mmHg, 60mmHg, and 90mmHg, respectively. Three days after high IOP treatment, loss of retinal ganglion cells (RGCs), formation of proinflammatory microglia/macrophages and neurotoxic astrocytes, and deposition of complement C3 in the retina were detected by immunofluorescence. ELISA was used to assess the protein levels of proinflammatory cytokines TNF and IL-1β in the retina. Results. Compared with young adult retinae, (1) loss of RGCs was more severe in aged retinae under the same IOP treatment, (2) microglia/macrophages were more prone to adopt proinflammatory phenotype in aged retinae in response to elevated IOP, (3) high IOP treatment induced astrogliosis, formation of neurotoxic astrocytes, and deposition of complement C3 more easily in aged retinae, and (4) aged retinae induced higher levels of proinflammatory cytokines TNF and IL-1β under the same IOP treatment. Conclusion. Our data indicated that aging affects the degree of retinal neuroinflammatory response initiated by ocular hypertension, which may contribute to the age-related susceptibility of RGCs to elevated IOP.