Peanut agglutinin binding glycoproteins in the chick retina: Their presence in Müller glia cells

1992 ◽  
Vol 31 (3) ◽  
pp. 532-542 ◽  
Author(s):  
C. Arregui ◽  
H. S. Barra ◽  
C. A. Landa
2016 ◽  
Vol 41 (7) ◽  
pp. 1797-1805 ◽  
Author(s):  
Ana María López-Colomé ◽  
Edith López ◽  
Orquidia G. Mendez-Flores ◽  
Arturo Ortega

Glia ◽  
2003 ◽  
Vol 44 (3) ◽  
pp. 251-263 ◽  
Author(s):  
Stefanie M. Hauck ◽  
Sabine Suppmann ◽  
Marius Ueffing

2015 ◽  
Vol 76 (9) ◽  
pp. 983-1002 ◽  
Author(s):  
Donika Gallina ◽  
Isabella Palazzo ◽  
Lillia Steffenson ◽  
Levi Todd ◽  
Andy J. Fischer

2016 ◽  
Vol 236 (4) ◽  
pp. 223-227 ◽  
Author(s):  
Gabriel Costa de Andrade ◽  
Christian Wertheimer ◽  
Kirsten Eibl ◽  
Armin Wolf ◽  
Anselm Kampik ◽  
...  

Stem Cells ◽  
2011 ◽  
Vol 29 (2) ◽  
pp. 344-356 ◽  
Author(s):  
Serena G. Giannelli ◽  
Gian Carlo Demontis ◽  
Grazia Pertile ◽  
Paolo Rama ◽  
Vania Broccoli

2006 ◽  
Vol 15 (18) ◽  
pp. 2659-2672 ◽  
Author(s):  
Agnes G.S.H. van Rossum ◽  
Wendy M. Aartsen ◽  
Jan Meuleman ◽  
Jan Klooster ◽  
Anna Malysheva ◽  
...  

2019 ◽  
Author(s):  
Isabella Palazzo ◽  
Kyle Deistler ◽  
Thanh V. Hoang ◽  
Seth Blackshaw ◽  
Andy J. Fischer

AbstractNeuronal regeneration in the retina is a robust, effective process in some cold-blooded vertebrates, but this process is ineffective in warm-blooded vertebrates. Understanding the mechanisms and cell-signaling pathways that restrict the reprogramming of Müller glia into proliferating neurogenic progenitors is key to harnessing the regenerative potential of the retina. Inflammation and reactive microglia are known to influence the formation of Müller glia-derived progenitor cells (MGPCs), but the mechanisms underlying this response are unknown. Using the chick retina in vivo as a model system, we investigate the role of the Nuclear Factor kappa B (NF-κB) signaling, a critical regulator of inflammation. We find that components of the NF-κB pathway are expressed by Müller glia and are dynamically regulated after neuronal damage or treatment with growth factors. Inhibition of NF-κB enhances, whereas activation suppresses the formation of proliferating MGPCs. Additionally, activation of NF-κB promotes glial differentiation from MGPCs in damaged retinas. With microglia ablated, the effects of NF-κB-agonists/antagonists on MGPC formation are reversed, suggesting that the context and timing of signals provided by reactive microglia influence how NF-κB-signaling impacts the reprogramming of Müller glia. We propose that NF-κB-signaling is an important signaling “hub” that suppresses the reprogramming of Müller glia into proliferating MGPCs and this “hub” coordinates signals provided by reactive microglia.


1985 ◽  
Vol 82 (16) ◽  
pp. 5570-5573 ◽  
Author(s):  
A. A. Moscona ◽  
L. Fox ◽  
J. Smith ◽  
L. Degenstein

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