Function and Mechanism of CNTF/LIF Signaling in Retinogenesis

Rhee, Kun Do; Yang, Xian-Jie

doi:10.1007/978-1-4419-1399-9_74

Cited by 22 publications

(21 citation statements)

References 41 publications

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“…Indeed, the silencing of PTPIP51 expression did not affect the generation of the CRX-positive photoreceptor precursors. This is in agreement with the down-regulation of PTPIP51 expression in P0 retinal explants treated with ciliary neurotrophic factor (Roger et al, 2007), where an inhibition of the rod photoreceptor differentiation was observed (Ezzeddine et al, 1997;Schulz-Key et al, 2002;Rhee et al, 2004;Rhee and Yang, 2010).…”

Section: Discussionsupporting

confidence: 82%

The protein tyrosine phosphatase interacting protein 51 (PTPIP51) is required for the differentiation of photoreceptors

et al. 2015

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Proliferation and differentiation of retinal progenitor cells (RPCs) are tightly controlled by extrinsic cues and distinct combinations of transcription factors leading to the generation of retinal cell type diversity. In this context, we investigated the role of the protein tyrosine phosphatase interacting protein 51 (PTPIP51) in the differentiation of RPCs. The expression pattern of PTPIP51 was analyzed by immunostaining during post-natal retinal development in the rat. Ex vivo electroporation has been used to silence or misexpress PTPIP51 in post-natal retinal explants, and the retinal phenotype was investigated after 3-7days in vitro (div). PTPIP51 expression in the retina started postnatally and was maintained throughout adulthood, especially in retinal ganglion cells and in the inner segment of photoreceptor cells. Silencing of Ptpip51 expression in postnatal retina failed to modify the commitment of late RPCs in the different lineages but severely impaired the final differentiation of photoreceptors, observed by a decrease in the fraction of Rhodopsin-positive cells after 7div. By contrast, misexpression of PTPIP51 in early or late RPCs failed to modify the differentiation of the RPCs. Our data demonstrate that PTPIP51 is implicated in the differentiation process of immature photoreceptors. Because PTPIP51 is specifically localized in the inner segment, PTPIP51 may contribute to the complex stage of maturation of the apical segment of these cells.

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Section: Discussionsupporting

confidence: 82%

The protein tyrosine phosphatase interacting protein 51 (PTPIP51) is required for the differentiation of photoreceptors

et al. 2015

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“…In addition, abnormal photoreceptor cell death or retinal injury results in reactive gliosis (Fisher and Lewis, 2003; Frasson et al, 1999), which is detected in Pten mutant retinas. Reactive Müller glial cells are known to secret growth factors such as LIF (Joly S, 2008), a member of the CNTF family of cytokines that promotes Müller glial fate (Goureau et al, 2004) and inhibits rod differentiation (Ezzeddine et al, 1997; Rhee et al, 2004; Rhee and Yang, 2010). Indeed, CNTF has been shown to induce the PI3K/Akt signaling cascade in zebrafish retina (Kassen et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

PTEN regulates retinal interneuron morphogenesis and synaptic layer formation

Sakagami

Chen

Nusinowitz

et al. 2012

Molecular and Cellular Neuroscience

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The lipid phosphatase PTEN is a critical negative regulator of extracellular signal-induced PI3K activities, yet the roles of PTEN in the neural retina remain poorly understood. Here, we investigate the function of PTEN during retinal development. Deletion of Pten at the onset of neurogenesis in retinal progenitors results in the reduction of retinal ganglion cells and rod photoreceptors, but increased Müller glial genesis. In addition, PTEN deficiency leads to elevated phosphorylation of Akt, especially in the developing inner plexiform layer, where high levels of PTEN are normally expressed. In Pten mutant retinas, various subtypes of amacrine cells show severe dendritic overgrowth, causing specific expansion of the inner plexiform layer. However, the outer plexiform layer remains relatively undisturbed in the Pten deficient retina. Physiological analysis detects reduced rod function and augmented oscillatory potentials originating from amacrine cells in Pten mutants. Furthermore, deleting Pten or elevating Akt activity in individual amacrine cells is sufficient to disrupt dendritic arborization, indicating that Pten activity is required cell autonomously to control neuronal morphology. Moreover, inhibiting endogenous Akt activity attenuates inner plexiform layer formation in vitro. Together, these findings demonstrate that suppression of PI3K/Akt signaling by PTEN is crucial for proper neuronal differentiation and normal retinal network formation.

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“…Ciliary neurotrophic factor (CNTF) CNTF exerts numerous effects on the development, differentiation and survival of retinal neurons (Rhee and Yang, 2010). The molecular mechanisms that explain the neuroprotective role of CNTF in the retina include: a direct action on photoreceptors to prevent apoptosis; the stimulation of Müller cells to produce photoreceptor survival factors (Zack, 2000); enhanced synthesis or distribution of glutamate transporters, thereby improving glutamate handling and resulting in less excitotoxic damage to retinal neurons (Escartin et al, 2006); and an induction of metabolic plasticity and increased resistance to metabolic damage (Escartin et al, 2007).…”

Section: Other Trophic Factorsmentioning

confidence: 99%

Glia–neuron interactions in the mammalian retina

Vecino

Rodríguez

Ruzafa

et al. 2016

Progress in Retinal and Eye Research

615

533

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The mammalian retina provides an excellent opportunity to study glia-neuron interactions and the interactions of glia with blood vessels. Three main types of glial cells are found in the mammalian retina that serve to maintain retinal homeostasis: astrocytes, Müller cells and resident microglia. Müller cells, astrocytes and microglia not only provide structural support but they are also involved in metabolism, the phagocytosis of neuronal debris, the release of certain transmitters and trophic factors and K(+) uptake. Astrocytes are mostly located in the nerve fibre layer and they accompany the blood vessels in the inner nuclear layer. Indeed, like Müller cells, astrocytic processes cover the blood vessels forming the retinal blood barrier and they fulfil a significant role in ion homeostasis. Among other activities, microglia can be stimulated to fulfil a macrophage function, as well as to interact with other glial cells and neurons by secreting growth factors. This review summarizes the main functional relationships between retinal glial cells and neurons, presenting a general picture of the retina recently modified based on experimental observations. The preferential involvement of the distinct glia cells in terms of the activity in the retina is discussed, for example, while Müller cells may serve as progenitors of retinal neurons, astrocytes and microglia are responsible for synaptic pruning. Since different types of glia participate together in certain activities in the retina, it is imperative to explore the order of redundancy and to explore the heterogeneity among these cells. Recent studies revealed the association of glia cell heterogeneity with specific functions. Finally, the neuroprotective effects of glia on photoreceptors and ganglion cells under normal and adverse conditions will also be explored.

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Function and Mechanism of CNTF/LIF Signaling in Retinogenesis

Cited by 22 publications

References 41 publications

The protein tyrosine phosphatase interacting protein 51 (PTPIP51) is required for the differentiation of photoreceptors

The protein tyrosine phosphatase interacting protein 51 (PTPIP51) is required for the differentiation of photoreceptors

PTEN regulates retinal interneuron morphogenesis and synaptic layer formation

Glia–neuron interactions in the mammalian retina

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