The characteristics of rat retinal Müller cells in high glucose, oxidative stress and hypoxia
LI Chunhua1 FENG Zhaohui2 ZHANG Xue1 TIAN Bingyu1 LEI Xiaoqin1 ZHOU Tingjie3 MA Weimei1
1.Department of Ophthalmology, Xi′an No.4 Hospital, Shaanxi Province, Xi′an 710004, China;
2.Department of Ophthalmology, the Second Affiliated Hospital of Xi′an Jiaotong University Medical College, Shaanxi Province, Xi′an 710004, China;
3.Xi′an Center for Disease Control and Prevention, Shaanxi Province, Xi′an 710054, China
Abstract：Objective To observe the characteristics of Sprague-Dawley (SD) rats retinal Müller cells under three pathological conditions including high glucose, oxidative stress and hypoxia, and to provide new research basis for the prevention and treatment of diabetic retinopathy. Methods SD rat retinal Müller cells were cultured in vitro and identified by glutathione synthetase (GS). The second generation of cells were divided into control group, high glucose group, oxidative stress group and hypoxia group randomly. The morphological changes of the cells were observed under inverted microscope, the changes of GS and α-smooth muscle actin (α-SMA) were observed by immunofluorescence staining, and the cell migration ability was observed by Transwell chamber. Results The Müller cells were successfully cultured and identified in vitro. In all groups, the function of Müller cells was impaired, and in oxidative stress group and hypoxia group, the structure was damaged, and the normal morphology was lost. In hypoxia group, the expression of α-SMA was positive, and the number of cells in the Transwell chamber was significantly higher than that in other groups, the differences were statistically significant (P ＜ 0.05). Conclusion High glucose, oxidative stress and hypoxia can destroy the function of Müller cells. Hypoxia can induce transforming into myofibroblast cells with migratory ability, which indicates that Müller cells are involved in the pathogenesis of proliferative diabetic retinopathy.
李春花1 冯朝晖2 张雪1 田冰玉1 雷晓琴1 周婷洁3 马为梅1. 大鼠视网膜M■ller细胞在高糖、氧化应激、缺氧中的表现[J]. 中国医药导报, 2019, 16(15): 18-20,40.
LI Chunhua1 FENG Zhaohui2 ZHANG Xue1 TIAN Bingyu1 LEI Xiaoqin1 ZHOU Tingjie3 MA Weimei1. The characteristics of rat retinal Müller cells in high glucose, oxidative stress and hypoxia. 中国医药导报, 2019, 16(15): 18-20,40.
[1] Hendrick AM，Gibson MV，Kulshreshtha A. Diabetic Retinopathy [J]. Prim Care，2015，42（3）：451-464.
[2] Ola MS，Nawaz MI，Siddiquei MM，et al. Recent advances in understanding the biochemical and molecular mechanism of diabetic retinopathy [J]. J Diabetes Complications，2015，74（1）：145-147.
[3] Wang SY，Andrews CA，Herman WH，et al. Incidence and Risk Factors for Developing Diabetic Retinopathy among Youths with Type 1 or Type 2 Diabetes throughout the United States [J]. Ophthalmology，2017，124（4）：424-430.
[4] Luna G，Lewis GP，Banna CD，et al. Expression profiles of nestin and synemin in reactive astrocytes and Müller cells following retinal injury：a comparison with glial fibrillar acidic protein and vimentin [J]. Mol Vis，2010，27（16）：2511-2523.
[5] Cutler RG. Oxidative stress profiling：part Ⅰ. Its potential importance in the optimization of human health [J]. Ann N Y Acad Sci，2005，1055：93-135.
[6] Capozzi ME，Mccollum GW，Cousins DB，et al. Linoleic Acid is a Diabetes-relevant Stimulator of Retinal Inflammation in Human Retinal Muller Cells and Microvascular Endothelial Cells [J]. J Diabetes Metab，2016，7（12）：718-723.
[7] Kim SJ，Yoo WS，Choi M，et al. Increased O-GlcNAcylation of NF-κB Enhances Retinal Ganglion Cell Death in Streptozotocin-induced Diabetic Retinopathy [J]. Curr Eye Res，2016，41（2）：249-257.
[8] Zhou T，Che D，Lan Y，et al. Mesenchymal marker expression is elevated in Müller cells exposed to high glucose and in animal models of diabetic retinopathy [J]. Oncotarget，2017，8（3）：4582-4594.
[9] Bringmann A，Pannicke T，Grosche J，et al. Müller cells in the healthy and diseased retina [J]. Prog Retin Eye Res，2006，25（4）：397-424.
[10] Reichenbach A，Wurm A，Pannicke T，et al. Muller cells as players in retinal degeneration and edema [J]. Graefes Arch Clin Exp Ophthalmol，2007，245（5）：627-636.
[11] Enger R，Gundersen GA，Haj-Yasein NN，et al. Molecular scaffolds underpinning macroglial polarization：an analysis of retinal Müller cells and brain astrocytes in mouse [J]. Glia，2012，60（12）：2018-2026.
[12] Guidry C. The role of Müller cells in fibrocontractive retinal disorders [J]. Prog Retin Eye Res，2005，24（1）：75-86.
[13] Cui Y，Xu X，Bi H，et al. Expression modification of uncoupling proteins and MnSOD in retinal endothelial cells and pericytes induced by high glucose：the role of reactive oxygen species in diabetic retinopathy [J]. Exp Eye Res，2006，83（4）：807-816.
[14] Zheng L，Du Y，Miller C，et al. Critical role of inducible nitric oxide synthase in degeneration of retinal capillaries in mice with streptozotocin-induced diabetes [J]. Diabetologia，2007，50（9）：1987-1996.
[15] Hao C，Weber AJ. Expression of glial fibrillary acidic protein and glutamine synthetase by Müller cells after optic nerve damage and intravitreal application of brain-derived neurotrophic factor [J]. Glia，2002，38（2）：115-125.
[16] Thompson K，Chen J，Luo Q，et al. Advanced glycation end（AGE）product modification of laminin downregulates Kir4.1 in retinal Müller cells [J]. PLoS One，2018，13（2）：1-13.
[17] Roigrevert MJ，Lleópérez A，Zanónmoreno V，et al. Enhanced Oxidative Stress and Other Potential Biomarkers for Retinopathy in Type 2 Diabetics：Beneficial Effects of the Nutraceutic Supplements [J]. Biomed Res Int，2015，4（12）：1-12.
[18] Kruk J，Kubasik-Kladna K，Aboul-Enein HY. The role oxidative stress in the pathogenesis of eye diseases：current status and a dual role of physical activity [J]. Mini Rev Med Chem，2015，16（3）：241-257.
[19] Abrahan CE，Insua MF，Politi LE，et al. Oxidative stress promotes proliferation and dedifferentiation of retina glial cells in vitro [J]. J Neurosci Res，2010，87（4）：964-977.
[20] Qu C，Cao W，Fan Y，et al. Near-Infrared Light Protect the Photoreceptor from Light-Induced Damage in Rats [J]. Adv Exp Med Bio，2010，664：365-374.
[21] Kumawat K，Koopmans T，Menzen MH，et al. Cooperative signaling by TGF-β1 and WNT-11 drives sm-α-actin expression in smooth muscle via Rho kinase-actin-MRTF-A signaling [J]. Am J Physiol Lung Cell Mol Physiol，2016，311（3）：529-537.
[22] 李冬平，原莉莉，张东昌.转化生长因子β2对人视网膜色素上皮细胞间质转化的影响[J].山西医药杂志，2017， 46（17）：2035-2037.
2019, Vol. 16 
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