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@#AIM: To analyze the function and mechanism of Apelin-13 in preventing the apoptosis of retinal Müller cells induced by hypoxia.<p>METHODS: In the research, the retinal Müller cells are regarded as research subjects, and the control group, hypoxia group and experiment group are set up. The cells of control group are cultivated in normal environment. The cells of hypoxia group are cultivated in hypoxia environment. The cells of experiment group are cultivated in hypoxia environment and are treated with the Apelin-13(1μmol/L). MTT method is used to monitor the changing of the cell viability, and the crystal violet staining method is adopted to observe the cell morphology. In addition, the immunofluorescence staining method is used to test the expression of GFAP and YAP and the TUNEL staining method is used to monitor the cell apoptosis situation and the apoptosis index is calculated. The protein staining method is used to observe the changing of the expression of p-LATS1, p-YAP, LATS1 and YAP protein. <p>RESULTS:The separated and extracted Müller cells grow on the wall and show elongation, polygon and circular shapes. The cytoplasm is plentiful and the cell nucleus show circular shape. The GFAP expression of the cell is positive. The treatment with 0.1, 1, 10μmol/L Apelin-13 can obviously prevent the Müller cell viability decreasing induced by hypoxia(<i>P</i><0.05 or <i>P</i><0.01). Compared with the control group, the cell apoptosis index of hypoxia group is obviously increased(<i>P</i><0.01). However, compared with the hypoxia group, the cell apoptosis index of experiment group is obviously decreased(<i>P</i><0.01). The p-LATS1 and p-YAP protein expression of the control group and hypoxia group does not have big difference. Compared with hypoxia group, the p-LATS1 and p-YAP protein expression of experiment group is obviously decreased(<i>P</i><0.01). The YAP protein expression of cell nucleus of control group and hypoxia group does not have great difference. Compared with hypoxia group, the cell nucleus expression of YAP cell is gretaly increased(<i>P</i><0.01). <p>CONCLUSION: Apelin-13 can be used to prevent the retinal Müller cells apoptosis caused by the hypoxia, which may be related to the regulation of YAP into the nucleus.
ABSTRACT
@#AIM: To analyze the function and mechanism of Apelin-13 in preventing the apoptosis of retinal Müller cells induced by hypoxia.<p>METHODS: In the research, the retinal Müller cells are regarded as research subjects, and the control group, hypoxia group and experiment group are set up. The cells of control group are cultivated in normal environment. The cells of hypoxia group are cultivated in hypoxia environment. The cells of experiment group are cultivated in hypoxia environment and are treated with the Apelin-13(1μmol/L). MTT method is used to monitor the changing of the cell viability, and the crystal violet staining method is adopted to observe the cell morphology. In addition, the immunofluorescence staining method is used to test the expression of GFAP and YAP and the TUNEL staining method is used to monitor the cell apoptosis situation and the apoptosis index is calculated. The protein staining method is used to observe the changing of the expression of p-LATS1, p-YAP, LATS1 and YAP protein. <p>RESULTS:The separated and extracted Müller cells grow on the wall and show elongation, polygon and circular shapes. The cytoplasm is plentiful and the cell nucleus show circular shape. The GFAP expression of the cell is positive. The treatment with 0.1, 1, 10μmol/L Apelin-13 can obviously prevent the Müller cell viability decreasing induced by hypoxia(<i>P</i><0.05 or <i>P</i><0.01). Compared with the control group, the cell apoptosis index of hypoxia group is obviously increased(<i>P</i><0.01). However, compared with the hypoxia group, the cell apoptosis index of experiment group is obviously decreased(<i>P</i><0.01). The p-LATS1 and p-YAP protein expression of the control group and hypoxia group does not have big difference. Compared with hypoxia group, the p-LATS1 and p-YAP protein expression of experiment group is obviously decreased(<i>P</i><0.01). The YAP protein expression of cell nucleus of control group and hypoxia group does not have great difference. Compared with hypoxia group, the cell nucleus expression of YAP cell is gretaly increased(<i>P</i><0.01). <p>CONCLUSION: Apelin-13 can be used to prevent the retinal Müller cells apoptosis caused by the hypoxia, which may be related to the regulation of YAP into the nucleus.
ABSTRACT
: With the increasing morbidity of diabetes, diabetic complications are also on the rise. Diabetic retinopathy is one of the severe complications in the late-stage diabetes. As a common blindness disease in clinic, diabetic retinopathy treatment has been a research focus. The pathogenesis of diabetic retinopathy is affected by multiple factors, multiple links and multiple genes, but the specific mechanism is not clear and it lacks effective drugs. This paper reviews the pathogenesis and treatment of risk factors of diabetic retinopathy and wish to provide reference for clinical prevention and treatment of DR.
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Retinal degenerative disease is the leading cause of visual loss,the mechanism is not clear and has no effective treatment method.In recent years,the field of stem cell research has made great progress.Stem cells have the potential of differentiating into all the body cells.Embryonic stem cells (ESCs) can be used to differentiate a variety of retinal cells,which has brought a new promise for the treatment of retinal degeneration disease.However,the most important step of this treatment is how to differentiate ESCs into photoreceptor cells and retinal pigment epithelium (RPF) cells.In this paper,we introduced the recent progress in the differentiation methods of ESCs into retinal cells,which contains spontaneous differentiation method,co-culture method,growth factors and small molecules induced method,adherent monoculture method,three dimensional differentiation method.
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Retinal pigment epithelium cells, retinal ganglial cells and photoreceptor cells play vital roles in maintaining the function of retina and choroid.Retinal cell death is the main cause of vision loss in ocular diseases.Necroptosis is a newly found way of programmed cell death.This article presented the mechanism of necroptosis and its research progess in different retinal diseases such as age-related macular degeneration and retinal detachment,which may provide new approaches for retinal diseases treatment.
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Purpose: To evaluate the effect of bevacizumab on the mitochondrial function of human retinal pigment epithelial (ARPE‑19), rat neurosensory retinal (R28) and human microvascular endothelial (HMVEC) cells in culture. Materials and Methods: ARPE‑19 and R28 cells were treated with 0.125, 0.25, 0.50 and 1 mg/ml of bevacizumab. The HMVEC cultures were treated with 0.125, 0.25, 0.50 and 1 mg/ml of bevacizumab or 1 mg/ml of immunoglobulin G (control). Mitochondrial function assessed by mitochondrial dehydrogenase activity (MDA) was determined using the WST‑1 assay. Results: Bevacizumab doses of 0.125 to 1 mg/ml for 5 days did not significantly affect the MDA of ARPE‑19 cells. Bevacizumab treatment at 0.125 and 0.25 mg/ml (clinical dose) did not significantly affect the MDA of R28 cells; however, 0.50 and 1 mg/ml doses significantly reduced the R28 cell mitochondrial function. All doses of bevacizumab significantly reduced the MDA of proliferating and non‑proliferating HMVEC. Conclusion: Bevacizumab exposure for 5 days was safe at clinical doses in both ARPE‑19 and R28 retinal neurosensory cells in culture. By contrast, bevacizumab exposure at all doses show a significant dose‑dependent decrease in mitochondrial activity in both the proliferating and non‑proliferating HMVEC in vitro. This suggests a selective action of bevacizumab on endothelial cells at clinical doses.
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Recent advances have seen a surge of new ideas and technologies to aid in the detection, treatment and further understanding of glaucoma. These technologies and advances are discussed to provide information on risk-factors, diagnosis and treatment. Glaucoma has never before seen such an advance in research and therapies coming forward in to the clinical workplace. It is an exciting time for physicians and researchers alike and over the next decade will certainly see advances in early detection, efficacious treatments and neuroprotection.
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We have investigated the growth and interactions between dissociated cells from different visual structures obtained from neonatal albino rats, namely, retina (R), superficial gray of the tectum (T), the lateral posterior portion of the dieneephalon (G), and occipital cortex (C). Dissociated cells obtained were either cultured separately or mixed with another cell type in 24-well plates coated with laminin. After 3 days of culture surviving cells were quantified by the MTT colorimetric microassay.The optical densities obtained from mixed cultures with cells from any two of the four types (G, R, T, C) of brain tissues were 1.3 to 3 times higher than the sum of their corresponding individual cultures except for those of G+C and T+G. Among them R+T and R+G were the most active cultures, followed by R+C and T+C. Further, condition medium from tectal cells (Tc) increased the activities of R and G for 3 and 2 times, respectively, and condition medium from retinal cells (Re) increased the activities of G and C for 1.3 and 2 times, respectively. Therefore it is suggested that neuronotrophic factors may be present in Tc and Rc.