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Inactive b1-integrin acts as a cell junction-localized molecular scaffold for Angiopoietin2-TIE2-FOXO1 signaling

ABSTRACT: Transcriptome profiling of lymphatic endothelial cells (LECs) treated with multimeric angiopoietin-2 (Ang2) for 3 or 6 hours to investigate early transcriptional responses.

ORGANISM(S): Homo sapiens

PROVIDER: GSE315536 | GEO | 2026/03/25

REPOSITORIES: GEO

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Inactive b1-integrin acts as a cell junction-localized molecular scaffold for Angiopoietin2-TIE2-FOXO1 signaling [RNA-Seq]

Project description:Transcriptome profiling of lymphatic endothelial cells (LECs) treated with R&D angiopoietin-2 (rhAng2) for 3 or 6 hours to investigate early transcriptional responses.

2026-03-25 | GSE316082 | GEO

Inactive b1-integrin acts as a cell junction-localized molecular scaffold for Angiopoietin2-TIE2-FOXO1 signaling

Project description:Inactive b1-integrin acts as a cell junction-localized molecular scaffold for Angiopoietin2-TIE2-FOXO1 signaling

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The angiopoietin-Tie2 pathway regulates Purkinje cell dendritic morphogenesis in a cell-autonomous manner

Project description:Neuro-vascular communication is essential to synchronize central nervous system development. Yet, the specific cellular players, defined developmental processes and molecular mechanisms involved in this crosstalk remain poorly characterized. Here we identify the angiopoietin/Tie2 signaling axis as a crucial regulator of dendritic morphogenesis of Purkinje cells (PC) during cerebellum development. We show that in the developing cerebellum Tie2 expression is not restricted to blood vessels but it is also in PCs. Its ligands angiopoietin-1 (Ang1) and angiopoietin-2 (Ang2) are expressed in neural cells and endothelial cells (ECs), respectively. PC-specific deletion of Tie2 results in reduced dendritic arborization, which is recapitulated in neural-specific Ang1-knockout and Ang2 full-knockout mice. Mechanistically, RNA sequencing reveals that Tie2 deficient PCs present alterations in gene expression of multiple genes involved in cytoskeleton organization, dendritic formation, growth and branching. Functionally, those morphological changes are accompanied by alterations in PC network electrophysiology. Altogether, our data propose that the Ang/Tie2 signaling axis serve as mediator of intercellular communication between neural cells, ECs and PCs, required to regulate PC dendritic morphogenesis and function.

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Inactive b1-integrin acts as a cell junction-localized molecular scaffold for Angiopoietin2-TIE2-FOXO1 signaling [RNA-Seq]

Project description:Inactive b1-integrin acts as a cell junction-localized molecular scaffold for Angiopoietin2-TIE2-FOXO1 signaling [RNA-Seq]

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RNA-Sequencing of HUVEC treated with Tie2 activating antibody

Project description:We analyzed genome-wide transcriptional changes induced by ABTAA+Ang2, using RNA-seq analysis of HUVECs Examination of 3 different antibodies treated to HUVEC to analyze the effect of Tie2 activation

2016-02-15 | E-GEOD-77597 | biostudies-arrayexpress

RNA-Sequencing of HUVEC treated with Tie2 activating antibody

Project description:We analyzed genome-wide transcriptional changes induced by ABTAA+Ang2, using RNA-seq analysis of HUVECs

2016-02-15 | GSE77597 | GEO

Effect of CVX-060 treatment on hepatic gene expression of cirrhotic rats

Project description:Currently, the therapeutic prospects for cirrhosis patients are limited to liver transplantation and, therefore, there is an urgent need to develop new therapeutic strategies for improved treatments. Cirrhosis was induced in male Wistar rats with CCl4 treatment, and RNA from the complete livers was extracted and quantified through microarray experiments. Angiopoietins signalling is a key pathway in blood vessel normalization. Angiopoietin 1 (Ang1)-Tie2 signalling stabilizes blood vessels, Angiopoietin 2 (Ang2) on the other hand is a context-dependent antagonist of Ang1 and decreases its stabilizing effect giving rise to immature blood vessels. Cirrhotic conditions are characterized by higher expression and activity of Ang2 than healthy conditions, resulting in the loss of blood vessels stability. Previous work showed that inhibition of Ang2 via CVX-060 enhances Ang1-Tie2 signalling, and can stabilize the vascular system in cirrhotic livers. We therefore performed RNA extraction after treatment of cirrhotic rats with CVX-060 during 4 weeks. We observed changes in expression state (expressed/not expressed) in key transcription factors previously implicated in cirrhosis.

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Project description:Angiopoietin-Tie1 signaling is required for lymphatic vascular integrity and both ANGPT2 and TIE1 genetic variants have been associated with lymphedema in patients1, 2. Concurrent with growth-factor signaling, mechanical forces sensed by lymphatic endothelial cells (LECs) are also needed to regulate lymphatics3, 4. How these two pathways might interact in the lymphatic system is unknown. Here, we identified a regulatory network in LECs linking activation of the mechanosensory channel, PIEZO1 to Angiopoietin-Tie signaling and repression of a downstream FOXO1 transcriptional response. RNAseq analysis of dermal LECs from Tie1-deficient embryos showed persistent FOXO1 activity with downregulation of LEC-associated genes including Ccl21a, Foxc2, Gata2 and Gja4, as well as increased expression of the mechanosensory channel, Piezo1. Activation of PIEZO1 in human dermal LECs (HDLECs) by the small molecule agonist, Yoda1, triggered exocytosis of the Tie ligand, Angiopoietin-2 (ANGPT2), activation of Tie/AKT/PI3K signaling and export of FOXO1 out of the nucleus. Our data identify a novel molecular pathway linking mechano-transduction to ANGPT2-Tie1 activity and dynamic modulation of FOXO1 activity needed for patterning and function of the lymphatic system

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Endothelial deletion of EPH receptor A4 alters single-cell profile and Tie2/Akap12 signaling to preserve blood-brain barrier integrity

Project description:Neurobiological consequences of traumatic brain injury (TBI) result from a complex interplay of secondary injury responses and sequela that mediates chronic disability. Endothelial cells are important regulators of the cerebrovascular response to TBI. Our work demonstrates that genetic deletion of endothelial cell (EC)-specific EPH receptor A4 (EphA4) using conditional EphA4f/f/Tie2-Cre and EphA4f/f/VE-Cadherin-CreERT2 knockout (KO) mice, promotes blood-brain barrier (BBB) integrity and tissue protection, which correlates with improved motor function and cerebral blood flow recovery following controlled cortical impact (CCI) injury. scRNAseq of capillary-derived KO ECs showed increased differential gene expression of BBB-related junctional and actin cytoskeletal regulators, namely, A-kinase anchor protein 12, Akap12, whose presence at Tie2 clustering domains is enhanced in KO microvessels. Transcript and protein analysis of CCI-injured whole cortical tissue or cortical-derived ECs suggests EphA4 limits the expression of Cldn5, Akt, and Akap12 and promotes Ang2. Blocking the Tie2 receptor using sTie2-Fc, attenuated BBB and tissue protection and reversed Akap12 mRNA and protein levels in KO compared to WT cortical-derived ECs. Conversely, direct stimulation of Tie2 using Vasculotide, an angiopoietin-1 memetic peptide, phenocopied the neuroprotection. Finally, we report a noteworthy rise in soluble Ang2 in the sera of individuals with acute TBI, highlighting its promising role as a vascular biomarker for early detection of BBB disruption. Overall, we describe a novel contribution of the axon guidance molecule, EphA4, in mediating TBI microvascular dysfunction through negative regulation of Tie2/Akap12 signaling.

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Single cell analysis in the adult aorta after Tie2 deletion

Project description:To analyze the Angiopoietin receptor Tie2 on the arterial endothelial cells during atheroclerosis

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