scholarly journals Otx2 enhances transdifferentiation of Müller cells‐derived retinal stem cells into photoreceptor‐like cells

2018 ◽  
Author(s):  
Yu Xiong ◽  
Hongpei Ji ◽  
Zhipeng You ◽  
Fei Yao ◽  
Rongrong Zhou ◽  
...  
Keyword(s):  
Stem Cells ◽  
Müller Cells ◽  
Muller Cells ◽  
Retinal Stem Cells

scholarly journals MiR-124 Promotes the Growth of Retinal Ganglion Cells Derived from Müller Cells

2018 ◽  
Vol 45 (3) ◽  
pp. 973-983 ◽  
Author(s):  
Ye He ◽  
Hai-bo Li ◽  
Xin Li ◽  
Yi Zhou ◽  
Xiao-bo Xia ◽  
...  
Keyword(s):  
Stem Cells ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Axon Growth ◽  
Müller Cells ◽  
Luciferase Assay ◽  
Control Group ◽  
Retinal Ganglion ◽  
Muller Cells ◽  
Retinal Stem Cells

Background/Aims: Retinal Müller cells could be induced to differentiate into retinal ganglion cells (RGCs), but RGCs derived from Müller cells have defects in axon growth, leading to a defect in signal conduction. In this study we aimed to explore the role of miR-124 in axon growth of RGCs derived from Müller cells. Methods: Müller cells were isolated from rat retina and induced to dedifferentiate into retinal stem cells. The stem cells were infected by PGC-FU-Atoh7-GFP lentivirus and then transfected with miR-124 or anti-miR-124, and the length of axon was compared. Furthermore, the cells were injected into the eyes of rat chronic ocular hypertension glaucoma model and axon growth in vivo was examined. The targeting of CoREST by miR-124 was detected by luciferase assay. Results: In retinal stem cells, the length of axon was 1,792±64.54 µm in miR-124 group, 509±21.35 µm in control group, and only 87.9±9.24 µm in anti-miR-124 group. In rat model, miR-124 promoted axon growth of RGCs differentiated from retinal stem cells. Furthermore, we found that miR-124 negatively regulated CoREST via directly targeting the binding site in CoREST 3′ UTR. Conclusions: We provide the first evidence that miR-124 regulates axon growth of RGCs derived from Müller cells, and miR-124 has translational potential for gene therapy of glaucoma.

scholarly journals ­­STAT3 combines with Rho-ROCK signaling pathway inhibitor, regulate axon growth of ganglion cells derived from retinal Müller cells

2020 ◽  
Author(s):  
xuezhi zhou ◽  
Yujue Wang ◽  
Manjuan Peng ◽  
Ye He ◽  
Jingjie Peng ◽  
...  
Keyword(s):  
Stem Cells ◽  
Layer Thickness ◽  
Axonal Regeneration ◽  
Axon Regeneration ◽  
Axon Growth ◽  
Müller Cells ◽  
Control Group ◽  
Marker Genes ◽  
Mrna Levels ◽  
Muller Cells

Abstract BackgroundMüller differentiated RGCs have potential therapeutic value for glaucoma. However, axonal regeneration of differentiated RGCs has been a difficult problem. Studies have confirmed that STAT3 and Y27632 play essential roles in regulating neuronal axon regeneration. Whether STAT3 and Y27632 can induce the Müller differentiated RGCs axon regeneration is still unknown.MethodRetina Müller cells were isolated and purified from Day 21 SD rats’ retina and were differentiated into retinal stem cells. The stem cells were randomly divided into five groups (control group, AAV-STAT3 group, shSTAT3 group, Y27632 group and AAV-STAT3 + Y27632 group). The axon length in each group were measured by ImageJ. Immunofluorescence were used to label the RGCs. The mRNA level of pluripotent associated and differentiation-associated proteins was analysed by qRT-PCR. Stem cells in different groups were injected into mice model of glaucoma. Immunohistochemical, Immunohistochemistry and OCT were performed to access RGC layer thickness in glaucoma model. VEP was used to detect the optic nerve conduction function.ResultsIn this study, we found that overexpression of STAT3 could promote the growth of RGCs axons generated by Müller cell differentiation. Combined with Y27632, axonal regeneration was significantly longer than that of the STAT3 group. However, after STAT3 was knocked out, axonal regeneration significantly decreased or even stopped. The mRNA levels of Esrrb, Prdm14, Sox2, and Rex1 in Müller differentiated RGCs after overexpression STAT3 combined with Y27632 were significantly increased, while the mRNA levels of Nestin, Eomes, Mixl1 and Gata4 were significantly decreased. The mRNA levels of Socs3, Pten, Klf9, and Mdm4 were significantly decreased, while the mRNA levels of Dclk2, Armcx1, C-MYC, and Nrn1 were significantly increased. The mRNA levels of differentiation and pluripotency marker genes showed opposite results after STAT3 deletion. After injecting Müller differentiated RGCs intervened by STAT3 combined with Y27632 into the eyes of the glaucoma model mice, the axon length, OCT displayed RGC layer thickness and the electrophysiology indicated by VEP were superior to those of the glaucoma model group.ConclusionsThese findings suggested that STAT3 combined with Y27632 can significantly improve the axonal growth level of RGCs, and reveal the potential mechanism to induce pluripotency of RGCs.

scholarly journals Human embryonic stem cells extracellular vesicles and their effects on immortalized human retinal Müller cells

PLoS ONE ◽  
2018 ◽  
Vol 13 (3) ◽  
pp. e0194004 ◽  
Author(s):  
Yingqian Peng ◽  
Edouard Baulier ◽  
Yifeng Ke ◽  
Alejandra Young ◽  
Novruz B. Ahmedli ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Extracellular Vesicles ◽  
Human Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Müller Cells ◽  
Muller Cells

K+ Channels of Müller Glial Cells in Retinal Disorders

2018 ◽  
Vol 17 (4) ◽  
pp. 255-260 ◽  
Author(s):  
Feng Gao ◽  
Lin-Jie Xu ◽  
Yuan Zhao ◽  
Xing-Huai Sun ◽  
Zhongfeng Wang
Keyword(s):  
Müller Cells ◽  
Major Type ◽  
Delayed Rectifier ◽  
Muller Cells ◽  
Bkca Channels ◽  
K Channels ◽  
Functional Changes ◽  
Physiological Properties ◽  
Retinal Disorders ◽  
Inwardly Rectifying

Background & Objective: Müller cell is the major type of glial cell in the vertebrate retina. Müller cells express various types of K+ channels, such as inwardly rectifying K+ (Kir) channels, big conductance Ca2+-activated K+ (BKCa) channels, delayed rectifier K+ channels (KDR), and transient A-type K+ channels. These K+ channels play important roles in maintaining physiological functions of Müller cells. Under some retinal pathological conditions, the changed expression and functions of K+ channels may contribute to retinal pathogenesis. Conclusion: In this article, we reviewed the physiological properties of K+ channels in retinal Müller cells and the functional changes of these channels in retinal disorders.

scholarly journals Melatonin attenuates oxidative stress and inflammation of Müller cells in diabetic retinopathy via activating the Sirt1 pathway

2021 ◽  
Vol 137 ◽  
pp. 111274
Author(s):  
Yuanyuan Tu ◽  
E Song ◽  
Zhenzhen Wang ◽  
Na Ji ◽  
Linling Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Retinopathy ◽  
Müller Cells ◽  
Muller Cells

Vitreous from idiopathic epiretinal membrane patients induces glial-to-mesenchymal transition in Müller cells

2021 ◽  
pp. 166181
Author(s):  
Adwaid Manu Krishna Chandran ◽  
Daniela Coltrini ◽  
Mirella Belleri ◽  
Sara Rezzola ◽  
Elena Gambicorti ◽  
...  
Keyword(s):  
Epiretinal Membrane ◽  
Müller Cells ◽  
Muller Cells ◽  
Mesenchymal Transition ◽  
Idiopathic Epiretinal Membrane

scholarly journals Muller cells are living optical fibers in the vertebrate retina

2007 ◽  
Vol 104 (20) ◽  
pp. 8287-8292 ◽  
Author(s):  
K. Franze ◽  
J. Grosche ◽  
S. N. Skatchkov ◽  
S. Schinkinger ◽  
C. Foja ◽  
...  
Keyword(s):  
Optical Fibers ◽  
Müller Cells ◽  
Muller Cells ◽  
Vertebrate Retina
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