Targeting Endostatin to Potentially Prevent Retinal Neovascularization Using a Hypoxia-Responsive Muller Glia Cell-Specific Gene Therapy

2014 ◽  
Vol 55 (12) ◽  
pp. 8054-8054 ◽  
Author(s):  
C. M. Craft
2002 ◽  
Vol 22 (21) ◽  
pp. 9228-9236 ◽  
Author(s):  
Takayuki Harada ◽  
Chikako Harada ◽  
Shinichi Kohsaka ◽  
Etsuko Wada ◽  
Kazuhiko Yoshida ◽  
...  

Mitochondrion ◽  
2017 ◽  
Vol 36 ◽  
pp. 52-59 ◽  
Author(s):  
Rupali Vohra ◽  
Iswariyaraja Sridevi Gurubaran ◽  
Ulrik Henriksen ◽  
Linda Hildegaard Bergersen ◽  
Lene Juel Rasmussen ◽  
...  

Science ◽  
2020 ◽  
Vol 370 (6519) ◽  
pp. eabb8598 ◽  
Author(s):  
Thanh Hoang ◽  
Jie Wang ◽  
Patrick Boyd ◽  
Fang Wang ◽  
Clayton Santiago ◽  
...  

Injury induces retinal Müller glia of certain cold-blooded vertebrates, but not those of mammals, to regenerate neurons. To identify gene regulatory networks that reprogram Müller glia into progenitor cells, we profiled changes in gene expression and chromatin accessibility in Müller glia from zebrafish, chick, and mice in response to different stimuli. We identified evolutionarily conserved and species-specific gene networks controlling glial quiescence, reactivity, and neurogenesis. In zebrafish and chick, the transition from quiescence to reactivity is essential for retinal regeneration, whereas in mice, a dedicated network suppresses neurogenic competence and restores quiescence. Disruption of nuclear factor I transcription factors, which maintain and restore quiescence, induces Müller glia to proliferate and generate neurons in adult mice after injury. These findings may aid in designing therapies to restore retinal neurons lost to degenerative diseases.


Gene Therapy ◽  
2014 ◽  
Vol 21 (6) ◽  
pp. 585-592 ◽  
Author(s):  
L C Byrne ◽  
B E Öztürk ◽  
T Lee ◽  
C Fortuny ◽  
M Visel ◽  
...  

2015 ◽  
Vol 144 (5) ◽  
pp. 443-455 ◽  
Author(s):  
Martina Kugler ◽  
Anja Schlecht ◽  
Rudolf Fuchshofer ◽  
Ingo Kleiter ◽  
Ludwig Aigner ◽  
...  

2019 ◽  
Author(s):  
Thanh Hoang ◽  
Jie Wang ◽  
Patrick Boyd ◽  
Fang Wang ◽  
Clayton Santiago ◽  
...  

AbstractInjury induces retinal Müller glia of cold-blooded, but not mammalian, vertebrates to regenerate neurons. To identify gene regulatory networks that control neuronal reprogramming in retinal glia, we comprehensively profiled injury-dependent changes in gene expression and chromatin accessibility in Müller glia from zebrafish, chick and mice using bulk RNA-Seq and ATAC-Seq, as well as single-cell RNA-Seq. Cross-species integrative analysis of these data, together with functional validation, identified evolutionarily conserved and species-specific gene networks controlling glial quiescence, gliosis and neurogenesis. In zebrafish and chick, transition from the resting state to gliosis is essential for initiation of retinal regeneration, while in mice a dedicated network suppresses neurogenic competence and restores quiescence. Selective disruption of NFI family transcription factors, which maintain and restore quiescence, enables Müller glia to proliferate and generate neurons in adult mice following retinal injury. These findings may aid in the design of cell-based therapies aimed at restoring retinal neurons lost to degenerative disease.Summary sentenceThis study identifies gene regulatory networks controlling proliferative and neurogenic competence in retinal Müller glia.


Glia ◽  
2007 ◽  
Vol 55 (14) ◽  
pp. 1486-1497 ◽  
Author(s):  
Serge A. van de Pavert ◽  
Alicia Sanz Sanz ◽  
Wendy M. Aartsen ◽  
Rogier M. Vos ◽  
Inge Versteeg ◽  
...  
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