Role of Müller cells in cone mosaic rearrangement in a rat model of retinitis pigmentosa

Glia ◽  
2011 ◽  
Vol 59 (7) ◽  
pp. 1107-1117 ◽  
Author(s):  
Eun-Jin Lee ◽  
Yerina Ji ◽  
Colleen L. Zhu ◽  
Norberto M. Grzywacz
PLoS ONE ◽  
2016 ◽  
Vol 11 (3) ◽  
pp. e0151668 ◽  
Author(s):  
Wan-Qing Yu ◽  
Yun Sung Eom ◽  
Jung-A Shin ◽  
Divya Nair ◽  
Sara X. Z. Grzywacz ◽  
...  

2011 ◽  
Vol 1382 ◽  
pp. 238-244 ◽  
Author(s):  
Shu Jia Huo (霍姝佳) ◽  
Ying Li (李英) ◽  
Geoffrey Raisman ◽  
Zheng Qin Yin (阴正勤)

2019 ◽  
Vol 98 (4) ◽  
Author(s):  
Andreas Bringmann ◽  
Tobias Duncker ◽  
Claudia Jochmann ◽  
Thomas Barth ◽  
Gernot I. W. Duncker ◽  
...  

2014 ◽  
Vol 56 (1) ◽  
pp. 352-364 ◽  
Author(s):  
Y. Ji ◽  
W.-Q. Yu ◽  
Y. S. Eom ◽  
F. Bruce ◽  
C. M. Craft ◽  
...  

1998 ◽  
Vol 15 (2) ◽  
pp. 211-218 ◽  
Author(s):  
ERIC M. WEXLER ◽  
OKSANA BERKOVICH ◽  
SCOTT NAWY

We have examined the role of neurotrophins in promoting survival of mammalian rod bipolar cells (RBC) in culture. Retinas taken from 8- to 10-day-old Long-Evans rats were dissociated and cultured in media supplemented with either nerve growth factor (NGF), neurotrophin-3 (NT-3), brain-derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF), or basic fibroblast growth factor (FGF-2). Survival was measured by the number of cells that were immunoreactive for α-, β-, γ-PKC, a bipolar cell-specific marker. Compared to untreated cultures, CNTF had no effect on RBC survival, while NGF and NT-3 increased survival only slightly. BDNF, however, increased survival by approximately 300%. Similar results were obtained with FGF-2. Both nerve growth factor (NGF) and an antibody (anti-REX) which interferes with binding to the 75-kD low-affinity neurotrophin receptor (p75NTR) eliminated BDNF-promoted survival, but had no effect on FGF-2-mediated survival. Interestingly, p75NTR was expressed by retinal glia (Müller cells), but not by the bipolar cells themselves, providing for the possibility that BDNF might induce Müller cells to produce a secondary factor, perhaps FGF-2, which directly rescues RBCs. In support of this hypothesis, an antibody that neutralizes FGF-2 attenuated the trophic effects of BDNF, and dramatically reduced survival in cultures with no added growth factors, indicating that there may be an endogenous source of FGF-2 that promotes survival of RBCs in culture. We suggest that BDNF increases production or release of FGF-2 by binding to p75NTR on Müller cells.


Neuroscience ◽  
1993 ◽  
Vol 55 (1) ◽  
pp. 291-301 ◽  
Author(s):  
S. Tout ◽  
T. Chan-Ling ◽  
H. Holländer ◽  
J. Stone

2011 ◽  
Vol 52 (13) ◽  
pp. 9527 ◽  
Author(s):  
Robert J. Walker ◽  
Nancy M. Anderson ◽  
Youde Jiang ◽  
Suleiman Bahouth ◽  
Jena J. Steinle

2010 ◽  
Vol 82 (1-2) ◽  
pp. 18-24 ◽  
Author(s):  
Lourdes Vidal ◽  
Florentina Díaz ◽  
Alicia Villena ◽  
Mercedes Moreno ◽  
José García Campos ◽  
...  

2019 ◽  
Vol 104 (4) ◽  
pp. 466-472 ◽  
Author(s):  
Andrea Govetto ◽  
Jean-Pierre Hubschman ◽  
David Sarraf ◽  
Marta S Figueroa ◽  
Ferdinando Bottoni ◽  
...  

BackgroundTo explore the role of foveal and parafoveal Müller cells in the morphology and pathophysiology of tractional macular disorders with a mathematical model of mechanical force transmission.MethodsIn this retrospective observational study, spectral-domain optical coherence tomography images of tractional lamellar macular holes and patients with myopic foveoschisis were reviewed and analysed with a mathematical model of force transmission. Parafoveal z-shaped Müller cells were modelled as a structure composed of three rigid rods, named R1, R2 and R3. The angle formed between the rods was referred to as θ . R1, R2 and R3 lengths as well as the variation of the angle θ were measured and correlated with best corrected visual acuity (BCVA).ResultsIn tractional lamellar macular holes, there was a significant reduction of the angle θ towards the foveal centre (p<0.001). By contrast, there were no significant differences in θ in myopic foveoschisis (p=0.570). R2 segments were more vertical in myopic foveoschisis. There was a significant association between lower θ angles at 200 µm temporal and nasal to the fovea and lower BCVA (p<0.001 and p=0.005, respectively). The stiffness of parafoveal Müller cells was predicted to be function of the angle θ , and it grew very rapidly as the θ decreased.ConclusionParafoveal Müller cells in the Henle fibre layer may guarantee structural stability of the parafovea by increasing retinal compliance and resistance to mechanical stress. Small values of the angle θ were related to worse BCVA possibly due to damage to Müller cell processes and photoreceptor’s axons.


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