scholarly journals Ciliary Neurotrophic Factor Promotes Müller Glia Differentiation from the Postnatal Retinal Progenitor Pool

2004 ◽  
Vol 26 (5-6) ◽  
pp. 359-370 ◽  
Author(s):  
Olivier Goureau ◽  
Kun Do Rhee ◽  
Xian-Jie Yang
Keyword(s):  
Neurotrophic Factor ◽  
Ciliary Neurotrophic Factor ◽  
Muller Glia ◽  
Müller Glia ◽  
Retinal Progenitor

scholarly journals Microglia–Müller Glia Cell Interactions Control Neurotrophic Factor Production during Light-Induced Retinal Degeneration

2002 ◽  
Vol 22 (21) ◽  
pp. 9228-9236 ◽  
Author(s):  
Takayuki Harada ◽  
Chikako Harada ◽  
Shinichi Kohsaka ◽  
Etsuko Wada ◽  
Kazuhiko Yoshida ◽  
...  
Keyword(s):  
Retinal Degeneration ◽  
Neurotrophic Factor ◽  
Cell Interactions ◽  
Muller Glia ◽  
Müller Glia ◽  
Glia Cell ◽  
Factor Production

scholarly journals Potential of Müller glia to become neurogenic retinal progenitor cells

Glia ◽  
2003 ◽  
Vol 43 (1) ◽  
pp. 70-76 ◽  
Author(s):  
Andy J. Fischer ◽  
Thomas A. Reh
Keyword(s):  
Progenitor Cells ◽  
Muller Glia ◽  
Müller Glia ◽  
Retinal Progenitor Cells ◽  
Retinal Progenitor

scholarly journals mTORC1-induced retinal progenitor cell overproliferation leads to accelerated mitotic aging and degeneration of descendent Müller glia

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Soyeon Lim ◽  
You-Joung Kim ◽  
Sooyeon Park ◽  
Ji-heon Choi ◽  
Younghoon Sung ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Tuberous Sclerosis Complex ◽  
Progenitor Cell ◽  
Mouse Retina ◽  
Muller Glia ◽  
Müller Glia ◽  
Retinal Progenitor ◽  
Mechanistic Target Of Rapamycin ◽  
Glycolytic Gene

Retinal progenitor cells (RPCs) divide in limited numbers to generate the cells comprising vertebrate retina. The molecular mechanism that leads RPC to the division limit, however, remains elusive. Here, we find that the hyperactivation of mechanistic target of rapamycin complex 1 (mTORC1) in an RPC subset by deletion of tuberous sclerosis complex 1 (Tsc1) makes the RPCs arrive at the division limit precociously and produce Müller glia (MG) that degenerate from senescence-associated cell death. We further show the hyperproliferation of Tsc1-deficient RPCs and the degeneration of MG in the mouse retina disappear by concomitant deletion of hypoxia-induced factor 1-a (Hif1a), which induces glycolytic gene expression to support mTORC1-induced RPC proliferation. Collectively, our results suggest that, by having mTORC1 constitutively active, an RPC divides and exhausts mitotic capacity faster than neighboring RPCs, and thus produces retinal cells that degenerate with aging-related changes.

scholarly journals rax, Hes1, and notch1 Promote the Formation of Müller Glia by Postnatal Retinal Progenitor Cells

Neuron ◽  
2000 ◽  
Vol 26 (2) ◽  
pp. 383-394 ◽  
Author(s):  
Takahisa Furukawa ◽  
Siddhartha Mukherjee ◽  
Zheng-Zheng Bao ◽  
Eric M. Morrow ◽  
Constance L. Cepko
Keyword(s):  
Progenitor Cells ◽  
Muller Glia ◽  
Müller Glia ◽  
Retinal Progenitor Cells ◽  
Retinal Progenitor

Preventing blindness in retinal disease: ciliary neurotrophic factor intraocular implants

2007 ◽  
Vol 42 (3) ◽  
pp. 399-402 ◽  
Author(s):  
Ian M. MacDonald ◽  
Yves Sauvé ◽  
Paul A. Sieving
Keyword(s):  
Neurotrophic Factor ◽  
Retinal Disease ◽  
Ciliary Neurotrophic Factor
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