scholarly journals Role of β-Adrenergic Receptor Regulation of TNF-α and Insulin Signaling in Retinal Müller Cells

2011 ◽  
Vol 52 (13) ◽  
pp. 9527 ◽  
Author(s):  
Robert J. Walker ◽  
Nancy M. Anderson ◽  
Youde Jiang ◽  
Suleiman Bahouth ◽  
Jena J. Steinle
Keyword(s):  
Insulin Signaling ◽  
Adrenergic Receptor ◽  
Müller Cells ◽  
Receptor Regulation ◽  
Muller Cells ◽  
Tnf Α

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 ◽  
...  
Keyword(s):  
Müller Cells ◽  
Spontaneous Closure ◽  
Muller Cells ◽  
Full Thickness ◽  
Macular Holes

Role of the low-affinity NGF receptor (p75) in survival of retinal bipolar cells

1998 ◽  
Vol 15 (2) ◽  
pp. 211-218 ◽  
Author(s):  
ERIC M. WEXLER ◽  
OKSANA BERKOVICH ◽  
SCOTT NAWY
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Neurotrophic Factor ◽  
Müller Cells ◽  
Bipolar Cells ◽  
Neurotrophin Receptor ◽  
Specific Marker ◽  
Muller Cells ◽  
Nerve Growth

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.

The role of müller cells in the formation of the blood-retinal barrier

Neuroscience ◽  
1993 ◽  
Vol 55 (1) ◽  
pp. 291-301 ◽  
Author(s):  
S. Tout ◽  
T. Chan-Ling ◽  
H. Holländer ◽  
J. Stone
Keyword(s):  
Müller Cells ◽  
Muller Cells ◽  
Blood Retinal Barrier

Abstract 15225: Post-ischemic Myocardial Insulin Resistance Induced by Tnf-α Overproduction Precipitates the Development of Heart Failure After Myocardial Infarction

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Feng Fu ◽  
Jia Li ◽  
Jie Xu ◽  
Yuan Zhang ◽  
Chao Gao ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Left Ventricular ◽  
Separate Experiment ◽  
Tnf Α ◽  
Lv Remodeling ◽  
Myocardial Insulin Resistance

Objectives: Clinical evidence has demonstrated a decreased myocardial insulin response in HF patients. However, the role of myocardial insulin resistance and the underlying mechanisms in HF are largely unclear. Methods and Results: Sprague Dawley rats subjected to myocardial infarction (MI) resulted in a progressive left ventricular (LV) remodeling and dysfunction. Echocardiographic assessment showed preserved LV end-systolic dimension (LVESD 0.453 ± 0.027 cm) and ejection fraction (EF 57.03 ± 2.35%) at 1 wk after MI, and evident LV dilation (LVESD 0.612 ± 0.026 cm) and dysfunction (EF 40.21 ± 3.09%) at 4 wk after MI. Myocardial insulin sensitivity decreased significantly at 1 wk after MI as evidenced by reduced insulin-stimulated myocardial fluorodeoxyglucose uptake (Standardized Uptake Value: 2.71 ± 0.42 vs. 5.13 ± 0.51 of sham+insulin, n=6, P <0.01) and GLUT-4 translocation and altered insulin signaling, whereas systemic insulin sensitivity remained unchanged. Mechanistically, myocardial TNF-α production was increased following MI. Treatment with etanercept (a TNF-α inhibitor) post-MI improved myocardial insulin sensitivity, while adenovirus-mediated overexpression of TNF-α resulted in myocardial insulin resistance in non-MI hearts. In addition, TNF-α overexpressed rat hearts exhibited LV dysfunction (EF 41.32 ± 4.21%) and LV dilation as early as 1 wk after MI. Moreover, insulin treatment during the first week following MI suppressed myocardial TNF-α production and increased myocardial insulin sensitivity, resulting in alleviated cardiac dysfunction and remodeling at 4 wk after MI. Importantly, in a separate experiment, cardiomyocyte-specific insulin receptor knockout mice exhibited aggravated post-ischemic LV remodeling and dysfunction compared with littermate controls. Conclusions: Our data provide novel insights that myocardial insulin resistance, independently of systemic insulin resistance, precipitates the development of post-ischemic HF. Myocardial insulin resistance is an early event partly attributed to myocardial TNF-α overproduction following MI. This finding indicates the essential role of myocardial insulin signaling in protection against ischemic HF.

Beta-adrenergic receptor signaling by the isomers of isoproterenol and like drugs in retinal endothelial cells and Müller cells

MedChemComm ◽  
2011 ◽  
Vol 2 (8) ◽  
pp. 726 ◽  
Author(s):  
Jayaprakash Pagadala ◽  
Kimberly Williams-Guy ◽  
Mohammed M. Nooh ◽  
Jena J. Steinle ◽  
Duane D. Miller
Keyword(s):  
Endothelial Cells ◽  
Adrenergic Receptor ◽  
Müller Cells ◽  
Receptor Signaling ◽  
Muller Cells ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Retinal Endothelial Cells

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
Keyword(s):  
Retinitis Pigmentosa ◽  
Rat Model ◽  
Müller Cells ◽  
Muller Cells ◽  
Cone Mosaic

scholarly journals The role of Müller cells in tractional macular disorders: an optical coherence tomography study and physical model of mechanical force transmission

2019 ◽  
Vol 104 (4) ◽  
pp. 466-472 ◽  
Author(s):  
Andrea Govetto ◽  
Jean-Pierre Hubschman ◽  
David Sarraf ◽  
Marta S Figueroa ◽  
Ferdinando Bottoni ◽  
...  
Keyword(s):  
Mathematical Model ◽  
Optical Coherence Tomography ◽  
Müller Cells ◽  
Mechanical Force ◽  
Optical Coherence ◽  
Muller Cells ◽  
Force Transmission ◽  
Myopic Foveoschisis ◽  
Macular Holes

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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