Macular hole following scleral buckling for rhegmatogenous retinal detachment: a case series.

BACKGROUND: Macular hole (MH) development following scleral buckling (SB) surgery for rhegmatogenous retinal detachment (RRD) repair is rare. This study presents both full-thickness MH (FTMH) and lamellar MH (LMH) cases following SB for the treatment of RRD. METHODS: Clinical records of patients undergoing SB surgery for treatment of RRD at the Xi'an People's Hospital (Xi'an Fourth Hospital) from January 2016 to December 2021 were reviewed, and cases with postoperative MH were selected. Clinical features and follow-up data were summarised, and possible causes were analysed. RESULTS: Among 483 identified cases (483 eyes), four eyes (three male patients, one female patient) had postoperative MH, with prevalence, mean age, and mean axial length of 0.83%, 43.5 ± 10.66 years, and 29.13 ± 3.80 mm, respectively. All patients did not undergo subretinal fluid (SRF) drainage. The mean time for detecting MH was 26 ± 15.5 days postoperatively. Macula-off RRD with high myopia and FTMH combined with retinal re-detachment were diagnosed in three patients. One patient had macula-on RRD with outer LMH. The average follow-up duration was 7.25 ± 1.5 months. The FTMH closed successfully after reoperation, while the outer LMH closed without intervention. Visual acuity insignificantly improved or slightly decreased in all patients. CONCLUSIONS: Patients with high myopia combined with macula-off RRD might be more susceptible to FTMH, causing MH related retinal detachment. Additionally, LMH following SB was noted in patients with macula-on RRD. Therefore, we should raise awareness of MH following SB for RRD repair.

MicroRNA-137 regulates hypoxia-induced retinal ganglion cell apoptosis through Notch1.

The apoptosis of retinal ganglion cells (RGCs) is a hallmark of several optic neuropathies. MicroRNAs (miRNAs) are recently identified regulators of various biological processes. However, the role of miRNAs in regulating RGC apoptosis remains largely unknown. We herein aimed to demonstrate that miR-137 acts as a hypoxia-responsive gene in RGCs that is downregulated under hypoxic conditions. It was observed that overexpression of miR-137 markedly aggravated hypoxia-induced cell apoptosis, whereas inhibition of miR-137 effectively protected RGCs against hypoxia-induced apoptosis. Hypoxia induced Notch1 expression and signaling activation, while blocking Notch signaling significantly aggravated hypoxia-induced cell apoptosis. Further data revealed that the pro-survival Akt signaling pathway was involved in miR-137-Notch signaling pathway-mediated RGC protection. Knockdown of Notch significantly reversed the effect of anti­miR-137 on RGC protection and Akt signaling activation. In addition, blocking Akt signaling also significantly abrogated the protective effect of anti-miR-137 on hypoxia-induced cell injury. Overall, the results of the present study demonstrated that miR-137 targets Notch1 expression, revealing a novel link between miR-137 and Notch signaling, and suggesting that a miR-137/Notch1 axis may serve as a potential molecular target for the treatment of hypoxia-induced retinal diseases.

MicroRNA-486-5p suppresses TGF-ß2-induced proliferation, invasion and epithelial-mesenchymal transition of lens epithelial cells by targeting Smad2.

The pathological development of lens epithelial cells (LECs) leads to posterior capsular opacification (PCO). This study was undertaken to investigate the effects of microRNA-486-5p (miR-486-5p) on TGF-ß2-induced proliferation, invasion and epithelial-mesenchymal transition (EMT) in the lens epithelial cell line SRA01/04, and to explore the underlying molecular mechanisms. The expression of miR-486-5p in TGF-ß2-induced SRA01/04 cells was down-regulated, and the expression of Smad2, p-Smad2 and p-Smad3 was up-regulated. A dual-luciferase reporter assay revealed that miR-486-5p directly targets the 30'-UTR of Smad2. MiR-486-5p mimic transfection markedly down-regulated the expression levels of Smad2, thus inhibiting the expression of p-Smad2 and p-Smad3. MiR-486-5p overexpression in SRA01/04 cells markedly suppressed TGF-ß2-induced proliferation and invasion, inhibited protein expression of CDK2 and CDK4, down-regulated fibronectin, α-SMA and vimentin and up-regulated E-cadherin; these effects were partly reversed by Smad2 overexpression. In short, these data show that miR-486-5p overexpression can inhibit TGF-ß2-induced proliferation, invasion and EMT in SRA01/04 cells by repressing Smad2/Smad3 signalling, implying that miR-486-5p may be an effective target to interfere in the progression of PCO.

Expressions of TGF-ß2, bFGF and ICAM-1 in lens epithelial cells of complicated cataract with silicone oil tamponade.

AIM: To investigate the expression differences of transforming growth factor-ß2 (TGF-ß2), basic fibroblast growth factor (bFGF) and intercellular cell-adhesion molecule-1 (ICAM-1) in lens epithelial cells (LECs) of complicated cataract with silicone oil tamponade and age-related cataract. METHODS: Totally 150 eyes of 150 patients (aged 35 to 77y) were investigated, including 75 patients with complicated cataract after silicone oil tamponade and 75 patients with age-related cataract. The central piece of anterior capsules was collected during cataract surgery. TGF-ß2, bFGF and ICAM-1 were detected in the 60 specimens of the two groups by immunohistochemistry. The expression levels of the three kinds of messenger ribonucleic acid (mRNA) were determined by real-time quantitative reverse transcription-polymerase chain reaction in the 90 specimens of the two groups. RESULTS: TGF-ß2 was detected in the cytomembrane and cytoplasm of the LECs and bFGF was detected in the nucleus. ICAM-1 was positive in the cytomembrane of the LECs and the distribution of positive cells was uneven. The mRNA genes expression of the TGF-ß2, bFGF and ICAM-1 was significant differences between the two groups and markedly increased in complicated cataract group (P<0.05). CONCLUSION: The up-regulated TGF-ß2, bFGF and ICAM-1 maybe associate with the occurrence and development of complicated cataract with silicone oil tamponade.

Crocin Inhibits Oxidative Stress and Pro-inflammatory Response of Microglial Cells Associated with Diabetic Retinopathy Through the Activation of PI3K/Akt Signaling Pathway.

Diabetic retinopathy (DR) is a serious microvascular complication of diabetes mellitus that is closely associated with the degeneration and loss of retinal ganglion cells (RGCs) caused by diabetic microangiopathy and subsequent oxidative stress and an inflammatory response. Microglial cells are classed as neurogliocytes and play a significant role in neurodegenerative diseases. Over-activated microglial cells may cause neurotoxicity and induce the death and apoptosis of RGCs. Crocin is one of the two most pharmacologically bioactive constituents in saffron. In the present study, we focused on the role of microglial cells in DR, suggesting that DR may cause the over-activation of microglial cells and induce oxidative stress and the release of pro-inflammatory factors. Microglial cells BV-2 and N9 were cultured, and high-glucose (HG) and free fatty acid (FFA) were used to simulate diabetes. The results showed that HG-FFA co-treatment caused the up-regulated expression of CD11b and Iba-1, indicating that BV-2 and N9 cells were over-activated. Moreover, oxidative stress markers and pro-inflammatory factors were significantly enhanced by HG-FFA treatment. We found that crocin prevented the oxidative stress and pro-inflammatory response induced by HG-FFA co-treatment. Moreover, using the PI3K/Akt inhibitor LY294002, we revealed that PI3K/Akt signaling plays a significant role in blocking oxidative stress, suppressing the pro-inflammatory response, and maintaining the neuroprotective effects of crocin. In total, these results provide a new insight into DR and DR-induced oxidative stress and the inflammatory response, which provide a potential therapeutic target for neuronal damage, vision loss, and other DR-induced complications.

Crocin Upregulates CX3CR1 Expression by Suppressing NF-κB/YY1 Signaling and Inhibiting Lipopolysaccharide-Induced Microglial Activation.

Glaucoma is a group of neurodegenerative diseases characterized by the progressive loss of retinal ganglion cells (RGCs) and optic nerve fibers. Microglial activation has been shown to be deleterious to RGCs and may participate in the progression of glaucoma. Crocin, one of the major active ingredients in saffron, has been found to inhibit microglial activation. However, the mechanism remains unclear. The aim of this study was to investigate whether crocin can inhibit lipopolysaccharide (LPS)-induced microglial activation and to clarify the mechanisms involved. The influence of crocin on primary RGCs and LPS-stimulated BV2 microglial cells survival was determined by the MTT and lactate dehydrogenase assays, or by flow cytometry. BV2 cells were pretreated with various concentrations of crocin for 2 h followed by 1 µg/mL LPS stimulation. Microglial markers and pro-inflammatory mediators were assessed by real-time PCR, western blot and ELISA. Furthermore, CX3CR1 expression was detected and the underlying mechanism was examined. The concentrations of crocin ranged from 0.1 to 1 µM, and did not show any cytotoxicity in RGC and BV2 cells. After crocin pretreatment, the expression of microglial markers (CD11b and Iba-1) and pro-inflammatory mediators (iNOS, COX-2, IL-1ß, and TNF-α) induced by LPS were significantly decreased in a dose-dependent manner. Additionally, CX3CR1 expression was remarkably increased by crocin via the suppression of NF-κB/Yin Yang 1 (YY1) signaling in BV2 cells. In conclusion, crocin effectively suppresses microglial activation and upregulates CX3CR1 expression by suppressing NF-κB/YY1 signaling.

[Effects of basic fibroblast growth factor composite sponge treated collagen on vascularization of orbital implants: a histopathologic analysis].

OBJECTIVE: To evaluate the effect of basic fibroblast growth factor (bFGF) treated collagen composite sponge on vascularization of HA orbital implants. METHODS: New Zealand rabbits received three different orbital implants:naked implants, implants wrapped with collagen composite sponge and implants wrapped with bFGF treated collagen composite sponge.Implants were harvested 2, 4, 6, 8 and 12 weeks after surgery. The vascularization of implants was then assessed by light and electron microscopy. RESULTS: At post-surgery weeks of 2, 4 and 6, bFGF treated collagen composite sponge induced the highest degree of vascularization of orbital implants. Collagen composite sponge alone resulted in higher extent of vascularization than naked implants. Complete vascularization of implants was observed at post-surgery 6 weeks by bFGF treated collagen composite sponge, which was not observed in the other two groups until post-surgery 8 weeks. There were significant differences in the average length of fibrovasculature and in the degree of vascularization among each group at post-surgery 2, 4 and 6 weeks (P<0.05), while no statistical difference was observed at post-surgery 8 and 12 weeks (P>0.05). CONCLUSIONS: bFGF treated collagen composite sponge facilitates fibrovascularization of orbital implants, and shortens the time required for complete vascularization. Collagen composite sponge alone promotes early-stage fibrovascularization, but fails to facilitate complete vascularization of orbital implants.