scholarly journals Spontaneous closure of small full‐thickness macular holes: Presumed role of Müller cells

2019 ◽  
Vol 98 (4) ◽  
Author(s):  
Andreas Bringmann ◽  
Tobias Duncker ◽  
Claudia Jochmann ◽  
Thomas Barth ◽  
Gernot I. W. Duncker ◽  
...  
2012 ◽  
Vol 90 ◽  
pp. 0-0
Author(s):  
M ZUEVA ◽  
V NEROEV ◽  
I TSAPENKO ◽  
P BYCHKOV ◽  
O SARYGINA

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.


2007 ◽  
Vol 51 (1) ◽  
pp. 76-77 ◽  
Author(s):  
Rika Hamano ◽  
Yukitoshi Shimoda ◽  
Shoji Kishi

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Xida Liang ◽  
Wu Liu

Idiopathic full-thickness macular hole is a severe visual impairment disease. Pars plana vitrectomy remains the primary treatment option for idiopathic full-thickness macular holes, and over 90% idiopathic full-thickness macular holes are closed by vitrectomy surgery. However, the full-thickness macular hole may close spontaneously, with a good visual acuity progress. Since recent studies are small-sample studies and case reports, the characteristics for spontaneous closure of idiopathic full-thickness macular holes are not fully understood. Here, we review the articles in PubMed database from 1999 to 2018 and discuss the characteristic and the risk factors, especially OCT structure features, for spontaneous closure of idiopathic full-thickness macular holes.


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

2006 ◽  
Vol 38 (4) ◽  
pp. 201-208 ◽  
Author(s):  
Tetsuya Sugiyama ◽  
Kozo Katsumura ◽  
Kimitoshi Nakamura ◽  
Masato Kobayashi ◽  
Michiko Muramatsu ◽  
...  

2015 ◽  
Vol 159 (6) ◽  
pp. 1142-1151.e3 ◽  
Author(s):  
Alexandre Matet ◽  
Maria Cristina Savastano ◽  
Marco Rispoli ◽  
Ciara Bergin ◽  
Alexandre Moulin ◽  
...  

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