Proteomic profiling of primary retinal Müller glia cells reveals a shift in expression patterns upon adaptation to in vitro conditions

Glia ◽  
2003 ◽  
Vol 44 (3) ◽  
pp. 251-263 ◽  
Author(s):  
Stefanie M. Hauck ◽  
Sabine Suppmann ◽  
Marius Ueffing
Keyword(s):  
Expression Patterns ◽  
Muller Glia ◽  
Müller Glia ◽  
Proteomic Profiling ◽  
Glia Cells

scholarly journals Müller glia cells regulate Notch signaling and retinal angiogenesis via the generation of 19,20-dihydroxydocosapentaenoic acid

2014 ◽  
Vol 211 (2) ◽  
pp. 281-295 ◽  
Author(s):  
Jiong Hu ◽  
Rüdiger Popp ◽  
Timo Frömel ◽  
Manuel Ehling ◽  
Khader Awwad ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Notch Signaling Pathway ◽  
Müller Cell ◽  
Muller Glia ◽  
Müller Glia ◽  
Lipid Profiling ◽  
Glia Cells ◽  
Retinal Angiogenesis ◽  
Muller Cell

Cytochrome P450 (CYP) epoxygenases generate bioactive lipid epoxides which can be further metabolized to supposedly less active diols by the soluble epoxide hydrolase (sEH). As the role of epoxides and diols in angiogenesis is unclear, we compared retinal vasculature development in wild-type and sEH−/− mice. Deletion of the sEH significantly delayed angiogenesis, tip cell, and filopodia formation, a phenomenon associated with activation of the Notch signaling pathway. In the retina, sEH was localized in Müller glia cells, and Müller cell–specific sEH deletion reproduced the sEH−/− retinal phenotype. Lipid profiling revealed that sEH deletion decreased retinal and Müller cell levels of 19,20–dihydroxydocosapentaenoic acid (DHDP), a diol of docosahexenoic acid (DHA). 19,20-DHDP suppressed endothelial Notch signaling in vitro via inhibition of the γ-secretase and the redistribution of presenilin 1 from lipid rafts. Moreover, 19,20-DHDP, but not the parent epoxide, was able to rescue the defective angiogenesis in sEH−/− mice as well as in animals lacking the Fbxw7 ubiquitin ligase, which demonstrate strong basal activity of the Notch signaling cascade. These studies demonstrate that retinal angiogenesis is regulated by a novel form of neuroretina–vascular interaction involving the sEH-dependent generation of a diol of DHA in Müller cells.

Glutamate Receptor Stimulation Up-Regulates Glutamate Uptake in Human Müller Glia Cells

2016 ◽  
Vol 41 (7) ◽  
pp. 1797-1805 ◽  
Author(s):  
Ana María López-Colomé ◽  
Edith López ◽  
Orquidia G. Mendez-Flores ◽  
Arturo Ortega
Keyword(s):  
Glutamate Receptor ◽  
Glutamate Uptake ◽  
Muller Glia ◽  
Müller Glia ◽  
Receptor Stimulation ◽  
Glia Cells

scholarly journals Pressure-dependent modulation of inward-rectifying K+ channels: implications for cation homeostasis and K+ dynamics in glaucoma

2019 ◽  
Vol 317 (2) ◽  
pp. C375-C389
Author(s):  
Rachel A. Fischer ◽  
Abigail L. Roux ◽  
Lauren K. Wareham ◽  
Rebecca M. Sappington
Keyword(s):  
Ganglion Cells ◽  
Primary Cultures ◽  
Elevated Pressure ◽  
Muller Glia ◽  
Müller Glia ◽  
Cation Homeostasis ◽  
K2p Channels ◽  
And Function

Glaucoma is the leading cause of blindness worldwide, resulting from degeneration of retinal ganglion cells (RGCs), which form the optic nerve. Prior to structural degeneration, RGCs exhibit physiological deficits. Müller glia provide homeostatic regulation of ions that supports RGC physiology through a process called K+ siphoning. Recent studies suggest that several retinal conditions, including glaucoma, involve changes in the expression of K+ channels in Müller glia. To clarify whether glaucoma-related stressors directly alter expression and function of K+ channels in Müller glia, we examined changes in the expression of inwardly rectifying K+ (Kir) channels and two-pore domain (K2P) channels in response to elevated intraocular pressure (IOP) in vivo and in vitro in primary cultures of Müller glia exposed to elevated hydrostatic pressure. We then measured outcomes of cell health, cation homeostasis, and cation flux in Müller glia cultures. Transcriptome analysis in a murine model of microbead-induced glaucoma revealed pressure-dependent downregulation of Kir and K2P channels in vivo. Changes in the expression and localization of Kir and K2P channels in response to elevated pressure were also found in Müller glia in vitro. Finally, we found that elevated pressure compromises the plasma membrane of Müller glia and induces cation dyshomeostasis that involves changes in ion flux through cation channels. Pressure-induced changes in cation flux precede both cation dyshomeostasis and membrane compromise. Our findings have implications for Müller glia responses to pressure-related conditions, i.e., glaucoma, and identify cation dyshomeostasis as a potential contributor to electrophysiological impairment observed in RGCs of glaucomatous retina.

scholarly journals Viability of Primary Human Pigment Epithelium Cells and Muller-Glia Cells after Intravitreal Ziv-Aflibercept and Aflibercept

2016 ◽  
Vol 236 (4) ◽  
pp. 223-227 ◽  
Author(s):  
Gabriel Costa de Andrade ◽  
Christian Wertheimer ◽  
Kirsten Eibl ◽  
Armin Wolf ◽  
Anselm Kampik ◽  
...  
Keyword(s):  
Pigment Epithelium ◽  
Muller Glia ◽  
Müller Glia ◽  
Glia Cells ◽  
Epithelium Cells

scholarly journals Adult Human Müller Glia Cells Are a Highly Efficient Source of Rod Photoreceptors

Stem Cells ◽  
2011 ◽  
Vol 29 (2) ◽  
pp. 344-356 ◽  
Author(s):  
Serena G. Giannelli ◽  
Gian Carlo Demontis ◽  
Grazia Pertile ◽  
Paolo Rama ◽  
Vania Broccoli
Keyword(s):  
Muller Glia ◽  
Müller Glia ◽  
Rod Photoreceptors ◽  
Glia Cells ◽  
Adult Human ◽  
Highly Efficient

scholarly journals Pals1/Mpp5 is required for correct localization of Crb1 at the subapical region in polarized Müller glia cells

2006 ◽  
Vol 15 (18) ◽  
pp. 2659-2672 ◽  
Author(s):  
Agnes G.S.H. van Rossum ◽  
Wendy M. Aartsen ◽  
Jan Meuleman ◽  
Jan Klooster ◽  
Anna Malysheva ◽  
...  
Keyword(s):  
Muller Glia ◽  
Müller Glia ◽  
Glia Cells ◽  
Subapical Region
Sign in / Sign up

Export Citation Format

Share Document