Neuroligin 1 induces blood vessel maturation by cooperating with the α6 integrin.

Samarelli, Anna Valeria; Riccitelli, E.; Bizzozero, Laura; Silveira, Tatiana N.; Seano, Giorgio; Pergolizzi, Margherita; Vitagliano, Grazia; Cascone, Ilaria; Carpentier, Gilles; Bottos, Alessia; Primo, Luca; Bussolino, Federico; Arese, Marco

doi:10.1074/jbc.a113.530972

Cited by 4 publications

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“…The number of branching points per field was quantified as described previously (Samarelli et al, 2014). Immunoreactivity was calculated as the surface area of each Ab staining co-localized with the EC markers endomucin, isolectin B4, or CD31 and normalized to the total vascular surface area visualized by the same molecules.…”

Section: Tissue and Cell Staining And Analysismentioning

confidence: 99%

“…Immunoreactivity was calculated as the surface area of each Ab staining co-localized with the EC markers endomucin, isolectin B4, or CD31 and normalized to the total vascular surface area visualized by the same molecules. The number of branching points per field was quantified as described previously (Samarelli et al, 2014).…”

Section: Tissue and Cell Staining And Analysismentioning

confidence: 99%

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TFEB controls vascular development by regulating the proliferation of endothelial cells

et al. 2018

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Transcription factor TFEB is thought to control cellular functions—including in the vascular bed—primarily via regulation of lysosomal biogenesis and autophagic flux. Here, we report that TFEB also orchestrates a non‐canonical program that controls the cell cycle/VEGFR2 pathway in the developing vasculature. In endothelial cells, TFEB depletion halts proliferation at the G1‐S transition by inhibiting the CDK4/Rb pathway. TFEB‐deficient cells attempt to compensate for this limitation by increasing VEGFR2 levels at the plasma membrane via microRNA‐mediated mechanisms and controlled membrane trafficking. TFEB stimulates expression of the miR‐15a/16‐1 cluster, which limits VEGFR2 transcript stability and negatively modulates expression of MYO1C, a regulator of VEGFR2 trafficking to the cell surface. Altered levels of miR‐15a/16‐1 and MYO1C in TFEB‐depleted cells cause increased expression of plasma membrane VEGFR2, but in a manner associated with low signaling strength. An endothelium‐specific Tfeb‐knockout mouse model displays defects in fetal and newborn mouse vasculature caused by reduced endothelial proliferation and by anomalous function of the VEGFR2 pathway. These previously unrecognized functions of TFEB expand its role beyond regulation of the autophagic pathway in the vascular system.

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Section: Tissue and Cell Staining And Analysismentioning

confidence: 99%

Section: Tissue and Cell Staining And Analysismentioning

confidence: 99%

TFEB controls vascular development by regulating the proliferation of endothelial cells

et al. 2018

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“…It will be important to examine the role of additional growth factors in this system. As for contactmediated guidance cues, many ECM components and interactors such as laminins (Gnanaguru et al, 2013), integrins (Hirota et al, 2011;Samarelli et al, 2014), dystrophin (Giocanti-Auregan et al, 2016), and proteoglycans (Stenzel et al, 2011) are very likely involved. However, their widespread expression makes these unlikely candidates to mediate a specific astrocyte-endothelial interaction.…”

Section: Patterning Of Retinal Blood Vesselsmentioning

confidence: 99%

Astrocytes follow ganglion cell axons to establish an angiogenic template during retinal development

O’Sullivan

Puñal

Kerstein

et al. 2017

Glia

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Immature astrocytes and blood vessels enter the developing mammalian retina at the optic nerve head, and migrate peripherally to colonize the entire retinal nerve fiber layer (RNFL). Retinal vascularization is arrested in retinopathy of prematurity (ROP), a major cause of bilateral blindness in children. Despite their importance in normal development and ROP, the factors that control vascularization of the retina remain poorly understood. Because astrocytes form a reticular network that appears to provide a substrate for migrating endothelial cells, they have long been proposed to guide angiogenesis. However, whether astrocytes do in fact impose a spatial pattern on developing vessels remains unclear, and how astrocytes themselves are guided is unknown. Here we explore the cellular mechanisms that ensure complete retinal coverage by astrocytes and blood vessels in mouse. We find that migrating astrocytes associate closely with the axons of retinal ganglion cells (RGCs), their neighbors in the RNFL. Analysis of Robo1; Robo2 mutants, in which RGC axon guidance is disrupted, and Math5 (Atoh7) mutants, which lack RGCs, reveals that RGCs provide directional information to migrating astrocytes that sets them on a centrifugal trajectory. Without this guidance, astrocytes exhibit polarization defects, fail to colonize the peripheral retina, and display abnormal fine-scale spatial patterning. Further, using cell type-specific chemical-genetic tools to selectively ablate astrocytes, we show that the astrocyte template is required for angiogenesis and vessel patterning. Our results are consistent with a model whereby RGC axons guide formation of an astrocytic network that subsequently directs vessel development.

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“…The Cell Adhesion Molecules (CAM) pathway also presents interesting signals, as we have identified a small cluster of 3 genes coding for neuroligins, which are neuronal proteins involved in the modulation of synaptic transmission (56). However, it has recently been shown that these genes are also involved in vascular processes (57,58). The NLGN1 gene thus seems to be a strong candidate for adaptation to high-altitude in Tibetans and Andeans and mechanisms linked to neuroligins action in angiogenesis at high altitude would deserve further investigation.…”

Section: New Insights Into Human Adaptation To Altitudementioning

confidence: 99%

Detecting gene subnetworks under selection in biological pathways

Gouy

Daub

Excoffier

2017

Preprint

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Advances in high throughput sequencing technologies have created a gap between data production and functional data analysis. Indeed, phenotypes result from interactions between numerous genes, but traditional methods treat loci independently, missing important knowledge brought by networklevel emerging properties. Therefore, evidencing selection acting on multiple genes affecting the evolution of complex traits remains challenging. In this context, gene network analysis provides a powerful framework to study the evolution of adaptive traits and facilitates the interpretation of genome-wide data. To tackle this problem, we developed a method to analyse gene networks that is suitable to evidence polygenic selection. The general idea is to search biological pathways for subnetworks of genes that directly interact with each other and that present unusual evolutionary features. Subnetwork search is a typical combinatorial optimization problem that we solve using a simulated annealing approach. We have applied our methodology to find signals of adaptation to high-altitude in human populations. We show that this adaptation has a clear polygenic basis and is influenced by many genetic components. Our approach improves on classical tests for selection based on single genes by identifying both new candidate genes and new biological processes involved in adaptation to altitude.

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Neuroligin 1 induces blood vessel maturation by cooperating with the α6 integrin.

Abstract: Authors are urged to introduce these corrections into any reprints they distribute. Secondary (abstract) services are urged to carry notice of these corrections as prominently as they carried the original abstracts.

Cited by 4 publications

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TFEB controls vascular development by regulating the proliferation of endothelial cells

TFEB controls vascular development by regulating the proliferation of endothelial cells

Astrocytes follow ganglion cell axons to establish an angiogenic template during retinal development

Detecting gene subnetworks under selection in biological pathways

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