RESUMEN
Diabetic retinopathy (DR) is one of the major causes of visual impairment and irreversible blindness in developed regions. Aside from abnormal angiogenesis, inflammation is the most specific and might be the initiating factor of DR. As a key participant in inflammation, interferon-gamma (IFN-γ) can be detected in different parts of the eye and is responsible for the breakdown of the blood-retina barrier and activation of inflammatory cells and other cytokines, which accelerate neovascularization and neuroglial degeneration. In addition, IFN-γ is involved in other vascular complications of diabetes mellitus and angiogenesis-dependent diseases, such as diabetic nephropathy, cerebral microbleeds, and age-related macular degeneration. Traditional treatments, such as anti-vascular endothelial growth factor agents, vitrectomy, and laser photocoagulation therapy, are more effective for angiogenesis and not tolerable for every patient. Many ongoing clinical trials are exploring effective drugs that target inflammation. For instance, IFN-α acts against viruses and angiogenesis and is commonly used to treat malignant tumors. Moreover, IFN-α has been shown to contribute to alleviating the progression of DR and other ocular diseases. In this review, we emphasize the roles that IFNs play in the pathogenesis of DR and discuss potential clinical applications of IFNs in DR, such as diagnosis, prognosis, and therapeutic treatment.
RESUMEN
AIM: To conduct a Meta-analysis for the change of interleukin-10 (IL-10) concentration in vitreous samples of patients with diabetic retinopathy (DR). METHODS: Systemic search for literature was conducted from the databases of PubMed, Web of Science and Cochrane Library by August 2019. Statistical analyses including standard mean difference (SMD) and its 95% confidence interval (CI) were performed by using RevMan 5.3 software. RESULTS: Totally 194 studies were screened and finally 11 studies were included in the Meta-analysis. The concentration of IL-10 in the DR group was higher than in the control group (P=0.003, SMD: 0.77, 95%CI: 0.25-1.28). Significant heterogeneity was found among all studies (P<0.00001, I 2=92%). The subgroup analysis showed that the concentration of IL-10 increased in vitreous samples from patients with DR compared to the non-DR controls (P=0.004, SMD: 1.44, 95%CI: 0.46-2.42). Moreover, the concentration of IL-10 in samples of proliferative diabetic retinopathy (PDR) patients was significantly higher than that of non-proliferative diabetic retinopathy (NPDR) patients (P=0.01, SMD: 0.61, 95%CI: 0.13-1.08). CONCLUSION: The vitreal concentration of IL-10 is significantly increased in patients with DR. Further studies are needed to reveal the mechanisms of IL-10 in DR.
RESUMEN
To evaluate the macular microstructure repair and explore the factors related to those changes and visual improvement after vitrectomy for idiopathic macular hole (IMH). Totally 19 eyes of 18 IMH patients who underwent macular hole (MH) surgery were evaluated with best-corrected visual acuity (BCVA) and spectral-domain optical coherence tomography (SD-OCT) images. All 19 eyes closed at 6mo postoperatively. BCVA was observed gradually improved (P<0.001), with subretinal fluid (SRF) gradually absorbed (P=0.021) and the rate of external limiting membrane (ELM) defects gradually decreased (P=0.011) with follow-up time. Poorer postoperative logMAR BCVA correlated with larger MH minimum diameter (P<0.001), larger MH basal diameter (P=0.008), longer symptom duration (P=0.002) and poorer preoperative logMAR BCVA (P=0.010). More improvement in BCVA correlated only with poorer preoperative in logMAR BCVA (P=0.002). The earlier reconstruction of ELM was associated with smaller MH basal diameter (P=0.022) and shorter symptom duration (P=0.008). In conclusion, smaller basal diameter of MH and shorter symptom duration were key factors in earlier reconstruction of ELM.
RESUMEN
AIM: To investigate the regulation and mechanisms of periostin expression in retinal Müller glia, and to explore the relevance to retinal neovascularization. METHODS: The oxygen-induced retinopathy (OIR) mouse model and the human Moorfield/Institute of Ophthalmology-Müller 1 (MIO-M1) cell line were used in the study. Immunofluorescence staining was used to determine the distribution and expression of periostin and a Müller glial cell marker glutamine synthetase (GS). Cytokines TNF-α and IFN-γ were added to stimulate the MIO-M1 cells. ShRNA was used to knockdown periostin expression in MIO-M1 cells. Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) was conducted to assess the mRNA expression of periostin. RESULTS: Immunofluorescence staining showed that periostin was expressed by MIO-M1 Müller glia. GS-positive Müller glia and periostin increased in OIR retinas, and were partially overlaid. The stimulation of TNF-α and IFN-γ reduced the mRNA expression of periostin significantly and dose-dependently in MIO-M1 cells. Knockdown of periostin reduced mRNA expression of vascular endothelial growth factor A (VEGFA) in MIO-M1 cells, while VEGFA expression was not changed in periostin knock-out OIR retinas. CONCLUSION: Müller glia could be one of the main sources of periostin in the retina, and might contribute to the pathogenesis of retinal neovascularization. Proinflammatory cytokines TNF-α and IFN-γ attenuate the periostin expression in retinal Müller glia, which provides a potential and novel method in treating retinal neovascular diseases.
