NFkB-signaling promotes glial reactivity and suppresses Muller glia-mediated neuron regeneration in the mammalian retina.

ABSTRACT: Müller glia (MG) in mammalian retinas are incapable of regenerating neurons after damage, whereas the MG in lower vertebrates regenerate functional neurons. Identification of cell signaling pathways and gene regulatory networks that regulate MG-mediated regeneration is key to harnessing the regenerative potential of MG. Here, we study how NFkB-signaling influences glial responses to damage and reprogramming of MG into neurons in the rodent retina. We find activation of NFkB and dynamic expression of NFkB-associated genes in MG after damage, however damage-induced NFkB activation is inhibited by microglia ablation. Knockout of NFkB in MG suppressed the accumulation of immune cells after damage. Inhibition of NFkB following NMDA-damage significantly enhanced the reprogramming of Ascl1-overex

SUBMITTER: Palazzo I 

PROVIDER: S-EPMC9585486 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature