scholarly journals Dynamic miRNA expression patterns during retinal regeneration in zebrafish: Reduced dicer or miRNA expression suppresses proliferation of Müller Glia‐derived neuronal progenitor cells

2014 ◽  
Vol 243 (12) ◽  
pp. 1591-1605 ◽  
Author(s):  
Kamya Rajaram ◽  
Rachel L. Harding ◽  
Travis Bailey ◽  
James G. Patton ◽  
David R. Hyde
Keyword(s):  
Progenitor Cells ◽  
Mirna Expression ◽  
Expression Patterns ◽  
Muller Glia ◽  
Müller Glia ◽  
Retinal Regeneration ◽  
Neuronal Progenitor Cells ◽  
Neuronal Progenitor

scholarly journals Midkine in chick and mouse retinas: neuroprotection, glial reactivity and the formation of Müller glia-derived progenitor cells

2020 ◽  
Author(s):  
Warren A. Campbell ◽  
Amanda Fritsch-Kelleher ◽  
Isabella Palazzo ◽  
Thanh Hoang ◽  
Seth Blackshaw ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Neuronal Survival ◽  
Expression Patterns ◽  
Model Systems ◽  
Muller Glia ◽  
Heparin Binding ◽  
Müller Glia ◽  
Related Factors ◽  
Neuroprotective Effects ◽  
Dying Cells

AbstractRecent studies have shown that midkine (MDK), a basic heparin-binding growth factor, is involved in the development and regeneration of the zebrafish retina. However, very little is known about MDK in the retinas of warm-blooded vertebrates. We investigate the expression patterns of MDK and related factors, roles in neuronal survival, and influence upon the formation of Müller glia-derived progenitor cells (MGPCs) in chick and mouse model systems. By using single-cell RNA-sequencing, we find that MDK is upregulated during Müller glia (MG) maturation in chick development and when stimulated to reprogram into MGPCs after NMDA damage or FGF2/Insulin treatment. Interestingly, MDK is significantly up-regulated by MG in damaged chick retinas, but down-regulated by MG in damaged mouse retinas. In both chick and mouse retinas, exogenous MDK selectively up-regulates cFOS and pS6 (a readout of mTOR-signaling) in MG. In the chick, intraocular injections of MDK before injury is neuroprotective with an observed decrease in dying neurons and microglial reactivity, inducing fewer proliferating MGPCs. Blocking MDK signaling with Na3VO4 following blocks neuroprotective effects with an increase the number of dying cells and negates the pro-proliferative effects on MGPCs. Inhibitors of PP2A and Pak1 associated with MDK integrin β1 signaling had MG specific inhibitory effects on MGPC formation. In mice, MDK administration with NMDA damage drives a small but significant increase in MGPCs. We conclude that MDK expression is dynamically regulated in reactive Müller glia and during reprogramming into MGPCs. MDK acts to coordinate glial activity, neuronal survival, and may act in an autocrine manner to influence the re-programming of Müller glia into proliferating MGPCs.

scholarly journals Cannabinoid signaling promotes the reprogramming of Muller glia into proliferating progenitor cells.

2021 ◽  
Author(s):  
Warren Campbell ◽  
Sydney Blum ◽  
Alana Reske ◽  
Thanh Hoang ◽  
Seth Blackshaw ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Expression Patterns ◽  
Synaptic Function ◽  
Muller Glia ◽  
Müller Glia ◽  
Rna Seq ◽  
Retinal Neurons ◽  
Pharmacological Agents ◽  
Retinal Microglia ◽  
Glial Reactivity

Endocannabinoids (eCB) are lipid-based neurotransmitters that are known to influence synaptic function in the visual system. eCBs are also known to suppress neuroinflammation in different pathological states. However, nothing is known about the roles of the eCB system during reprogramming of Müller glia (MG) into proliferating progenitor-like cells in the retina. Accordingly, we used the chick and mouse model to characterize expression patterns of eCB-related genes and applied pharmacological agents to examine how the eCB system impacts glial reactivity and the capacity of MG to become Müller glia-derived progenitor cells (MGPCs). We probed single cell RNA-seq libraries to identify eCB-related genes and identify cells with dynamic patterns of expression in damaged retinas. MG and inner retinal neurons expressed the eCB receptor CNR1, as well as enzymes involved in eCB metabolism. In the chick, intraocular injections of 2-Arachidonoylglycerol (2-AG) and Anandamide (AEA) potentiated the formation of MGPCs. Consistent with these findings, CNR1-agonists and MGLL-inhibitor promoted reprogramming, whereas CNR1-antagonist and inhibitors of eCB synthesis suppressed reprogramming. Surprisingly, retinal microglia were largely unaffected by increases or decreases in eCB signaling in both chick and mouse models. However, eCB-signaling suppressed the activation of NFkB-reporter in MG in damaged mouse retinas. We conclude that the eCB system in the retina influences the reactivity of MG and is important for regulating glial reactivity and the reprogramming of MG into proliferating MGPCs, but not for regulating the reactivity of immune cells in the retina.

Müller Glia-Mediated Retinal Regeneration

2021 ◽  
Author(s):  
Hui Gao ◽  
Luodan A ◽  
Xiaona Huang ◽  
Xi Chen ◽  
Haiwei Xu
Keyword(s):  
Muller Glia ◽  
Müller Glia ◽  
Retinal Regeneration

scholarly journals RNase A Promotes Proliferation of Neuronal Progenitor Cells via an ERK-Dependent Pathway

2018 ◽  
Vol 11 ◽  
Author(s):  
Hsin-Yu Liu ◽  
Chiung-Ya Chen ◽  
Yun-Fen Hung ◽  
Hong-Ru Lin ◽  
Hsu-Wen Chao ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Rnase A ◽  
Neuronal Progenitor Cells ◽  
Neuronal Progenitor ◽  
Dependent Pathway
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