N-cadherin-based adherens junction regulates the maintenance, proliferation, and differentiation of neural progenitor cells during development

Miyamoto, Yasunori; Sakane, Fumi; Hashimoto, Kei

doi:10.1080/19336918.2015.1005466

Cited by 93 publications

(74 citation statements)

References 143 publications

(257 reference statements)

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“…Because N‐cadherin‐mediated contacts participate to the maintenance of neuroepithelial progenitors in the ventricular zone , such defects further argue that PrP C deficiency impacts on the proper expansion of the neural stem cell pool. In addition, in view of the link between cadherin‐dependent contacts and β‐catenin signaling , these data suggest that the lack of PrP C affects the pool of β‐catenin in neural stem and/or progenitor cells of the neuroepithelium, which may in turn impact on their proliferation/differentiation balance. Altogether, these findings add to the complex interplay between PrP C and cadherins, since PrP C was previously shown to contribute to the recruitment of E‐cadherin at cell‐cell contacts or to the trafficking of N‐cadherin in differentiating neurons .…”

Section: Discussionmentioning

confidence: 90%

The Cellular Prion Protein Controls Notch Signaling in Neural Stem/Progenitor Cells

et al. 2016

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The prion protein is infamous for its involvement in a group of neurodegenerative diseases known as Transmissible Spongiform Encephalopathies. In the longstanding quest to decipher the physiological function of its cellular isoform, PrP , the discovery of its participation to the self-renewal of hematopoietic and neural stem cells has cast a new spotlight on its potential role in stem cell biology. However, still little is known on the cellular and molecular mechanisms at play. Here, by combining in vitro and in vivo murine models of PrP depletion, we establish that PrP deficiency severely affects the Notch pathway, which plays a major role in neural stem cell maintenance. We document that the absence of PrP in a neuroepithelial cell line or in primary neurospheres is associated with drastically reduced expression of Notch ligands and receptors, resulting in decreased levels of Notch target genes. Similar alterations of the Notch pathway are recovered in the neuroepithelium of Prnp embryos during a developmental window encompassing neural tube closure. In addition, in line with Notch defects, our data show that the absence of PrP results in altered expression of Nestin and Olig2 as well as N-cadherin distribution. We further provide evidence that PrP controls the expression of the epidermal growth factor receptor (EGFR) downstream from Notch. Finally, we unveil a negative feedback action of EGFR on both Notch and PrP . As a whole, our study delineates a molecular scenario through which PrP takes part to the self-renewal of neural stem and progenitor cells. Stem Cells 2017;35:754-765.

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Section: Discussionmentioning

confidence: 90%

The Cellular Prion Protein Controls Notch Signaling in Neural Stem/Progenitor Cells

et al. 2016

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“…Cerebrospinal fluid is primarily produced in the choroid plexuses, which consist of many capillaries and are important components of the blood‐CSF barrier . VE‐cadherin is a crucial component of adherent junctions (AJs) in vascular endothelial cells, which regulates water and solutes in and out vessels and forms the restrictive endothelial barrier . VE‐cadherin possesses a general modular structure of five extracellular repeats, a transmembrane domain, and a cytoplasmic tail .…”

Section: Discussionmentioning

confidence: 99%

“…11 VE-cadherin is a crucial component of adherent junctions (AJs) in vascular endothelial cells, which regulates water and solutes in and out vessels 34 and forms the restrictive endothelial barrier. 34,35 VE-cadherin possesses a general modular structure of five extracellular repeats, a transmembrane domain, and a cytoplasmic tail. 36 The external domain of VE-cadherin mediates homophilic binding, 36,37 while the cytoplasmic domain of VE-cadherin interacts with catenin proteins which prevent VE-cadherin proteolysis.…”

Section: Discussionmentioning

confidence: 99%

Thrombin disrupts vascular endothelial‐cadherin and leads to hydrocephalus via protease‐activated receptors‐1 pathway

Hao

Zhang

et al. 2019

CNS Neurosci Ther

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Summary Aims Previous studies indicated that intraventricular injection of thrombin would induce hydrocephalus. But how thrombin works in this process remains unclear. Since cadherin plays a critical role in hydrocephalus, we aimed to explore the mechanisms of how thrombin acted on choroid plexus vascular endothelium and how thrombin interacted with vascular endothelial‐cadherin (VE‐cadherin) during hydrocephalus. Methods There were two parts in this study. Firstly, rats received an injection of saline or thrombin into the right lateral ventricle. Magnetic resonance imaging was applied to measure the lateral ventricle volumes. Albumin leakage and Evans blue content were assessed to test the blood‐brain barrier function. Immunofluorescence and Western blot were applied to detect the location and the expression of VE‐cadherin. Secondly, we observed the roles of protease‐activated receptors‐1 (PAR1) inhibitor (SCH79797), Src inhibitor (PP2), p21‐activated kinase‐1 (PAK1) inhibitor (IPA3) in the thrombin‐induced hydrocephalus, and their effects on the regulation of VE‐cadherin. Results Our study demonstrated that intraventricular injection of thrombin caused significant downregulation of VE‐cadherin in choroid plexus and dilation of ventricles. In addition, the inhibition of PAR1/p‐Src/p‐PAK1 pathway reversed the decrease of VE‐cadherin and attenuated thrombin‐induced hydrocephalus. Conclusions Our results suggested that the thrombin‐induced hydrocephalus was associated with the inhibition of VE‐cadherin via the PAR1/p‐Src/p‐PAK1 pathway.

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“…During early stages of development, retinal progenitor cells (RPCs) organize into a pseudostratified epithelium and exhibit the apical-basal polarity (20,21). The polarity of RPCs is essential for the morphogenesis of retina, which depends on the proper expression and distribution of proteins that constitute the apical junctional (AJ) complex (22,23). On the one hand, polarity and adhesion proteins participate in the establishment and maintenance of the retinal architecture.…”

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confidence: 99%

S1P transporter SPNS2 regulates proper postnatal retinal morphogenesis

et al. 2018

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Spinster homolog 2 (SPNS2) is the membrane transporter of sphingosine-1-phosphate (S1P), and it participates in several physiologic processes by activating different S1P receptors (S1PRs). However, its functions in the nervous system remain largely unclear. We explored the important role of SPNS2 in the process of retinal morphogenesis using a spns2-deficient rat model. In the absence of the functional SPNS2 transporter, we observed progressively aggravating laminar disorganization of the epithelium at the postnatal stage of retinal development. Disrupted cell polarity, delayed cell-cycle exit of retinal progenitor cells, and insufficient migration of newborn neurons were proposed in this study as potential mechanisms accounting for this structural disorder. In addition, we analyzed the expression profiles of spns2 and s1prs, and proposed that SPNS2 regulated retinal morphogenesis by establishing the S1P level in the eye and activating S1PR3 signaling. These data indicate that SPNS2 is indispensable for normal retinal morphogenesis and provide new insights on the role of S1P in the developing retina using an established in vivo model.-Fang, C., Bian, G., Ren, P., Xiang, J., Song, J., Yu, C., Zhang, Q., Liu, L., Chen, K., Liu, F., Zhang, K., Wu, C., Sun, R., Hu, D., Ju, G., Wang, J. S1P transporter SPNS2 regulates proper postnatal retinal morphogenesis.

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N-cadherin-based adherens junction regulates the maintenance, proliferation, and differentiation of neural progenitor cells during development

Cited by 93 publications

References 143 publications

The Cellular Prion Protein Controls Notch Signaling in Neural Stem/Progenitor Cells

The Cellular Prion Protein Controls Notch Signaling in Neural Stem/Progenitor Cells

Thrombin disrupts vascular endothelial‐cadherin and leads to hydrocephalus via protease‐activated receptors‐1 pathway

S1P transporter SPNS2 regulates proper postnatal retinal morphogenesis

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