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In-depth proteomics identifies a role for autophagy in controlling ROS-mediated endothelial barrier permeability

ABSTRACT: We have used in-depth quantitative proteomics to identify processes required for the formation/maintenance of a stable new vessel. To do that we have used SILAC-based proteomics and a simple in vitro humam endothelial cell model that recapitulates vessel formation in vivo.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Vessel, Blood Vessel Endothelial Cell

SUBMITTER: Sara Zanivan

LAB HEAD: Sara Zanivan

PROVIDER: PXD003284 | Pride | 2016-06-07

REPOSITORIES: Pride

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			Action	DRS
	20121022_VelosProElite_FrPa_HUVEC_ConfluentProt_sc1_24h_pH11.raw	Raw
	20121022_VelosProElite_FrPa_HUVEC_ConfluentProt_sc1_24h_pH3.raw	Raw
	20121022_VelosProElite_FrPa_HUVEC_ConfluentProt_sc1_24h_pH4.raw	Raw
	20121022_VelosProElite_FrPa_HUVEC_ConfluentProt_sc1_24h_pH5.raw	Raw
	20121022_VelosProElite_FrPa_HUVEC_ConfluentProt_sc1_24h_pH6.raw	Raw

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Publications

In-Depth Proteomics Identifies a Role for Autophagy in Controlling Reactive Oxygen Species Mediated Endothelial Permeability.

Patella Francesca F Neilson Lisa J LJ Athineos Dimitris D Erami Zahra Z Anderson Kurt I KI Blyth Karen K Ryan Kevin M KM Zanivan Sara S

Journal of proteome research 20160615 7

Endothelial cells (ECs) form the inner layer of blood vessels and physically separate the blood from the surrounding tissue. To support tissues with nutrients and oxygen, the endothelial monolayer is semipermeable. When EC permeability is altered, blood vessels are not functional, and this is associated with disease. A comprehensive knowledge of the mechanisms regulating EC permeability is key in developing strategies to target this mechanism in pathologies. Here we have used an in vitro model o ...[more]

PMID: 27246970

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Physiological Vascular Permeability Requires Induction of Endothelial NR4A1 by Progesterone Receptor [RNA-Seq]

Project description:Vascular permeability is frequently associated with inflammation and it is triggered by chemokines and by a cohort of secreted permeability factors, such as VEGF. In contrast, here we showed that the physiological vascular permeability that precedes implantation is directly controlled by progesterone receptor (PR) and it is independent of VEGF. Both global and endothelial-specific deletion of PR block physiological vascular permeability in the uterus while misexpression of PR in the endothelium of other organs results in ectopic vascular leakage. Integration of genome-wide transcriptional profile of endothelium and ChIP-sequencing revealed that PR induces a NR4A1 (Nur77/TR3) specific transcriptional program that broadly regulates vascular permeability in response to progesterone. This program triggers concurrent suppression of several junctional proteins and leads to an effective, timely and venule-specific regulation of vascular barrier function. Silencing NR4A1 blocks PR-mediated permeability responses indicating a direct link between PR and NR4A1. These results reveal a previously unknown function for progesterone receptor on endothelial cell biology with consequences to physiological vascular permeability and implications to the clinical use of progestins and anti-progestins on blood vessel integrity. Examination of PR target genes in human umbilical vein endothelial cells (HUVECs) using RNA-seq (PR infected only -PR only and PR infected followed by ligand treatment-PR+P)

2014-01-01 | E-GEOD-43788 | biostudies-arrayexpress

Physiological Vascular Permeability Requires Induction of Endothelial NR4A1 by Progesterone Receptor [ChIP-Seq]

Project description:Vascular permeability is frequently associated with inflammation and it is triggered by chemokines and by a cohort of secreted permeability factors, such as VEGF. In contrast, here we showed that the physiological vascular permeability that precedes implantation is directly controlled by progesterone receptor (PR) and it is independent of VEGF. Both global and endothelial-specific deletion of PR block physiological vascular permeability in the uterus while misexpression of PR in the endothelium of other organs results in ectopic vascular leakage. Integration of genome-wide transcriptional profile of endothelium and ChIP-sequencing revealed that PR induces a NR4A1 (Nur77/TR3) specific transcriptional program that broadly regulates vascular permeability in response to progesterone. This program triggers concurrent suppression of several junctional proteins and leads to an effective, timely and venule-specific regulation of vascular barrier function. Silencing NR4A1 blocks PR-mediated permeability responses indicating a direct link between PR and NR4A1. These results reveal a previously unknown function for progesterone receptor on endothelial cell biology with consequences to physiological vascular permeability and implications to the clinical use of progestins and anti-progestins on blood vessel integrity. Examination of PR binding sites in HUVEC cells using ChIP-seq (non-infected-negative control, PR infected followed by ligand treatment-PR+P or vehicle PR)

2014-01-01 | E-GEOD-43786 | biostudies-arrayexpress

Profiling of purified autophagic vesicle content and degradome in the maturing and aging brain - Part II

Project description:In this second part of the project “Profiling of purified autophagic vesicle content and degradome in the maturing and aging brain” four label-free proteomics studies were performed to characterize stabilization of potential autophagy targets upon lysosomal and/or autophagy inhibition.

2023-08-07 | PXD041376 | Pride

Distinct signal transduction pathways downstream of the (P)RR revealed by microarray and ChIP-chip analyses [Expt: Geni_Bafi]

Project description:Within the overall project, we performed a set of microarray and chromatin-immunoprecipitation (ChIP)-chip experiments using siRNA against the (pro)renin receptor ((P)RR), stable overexpression of PLZF, the PLZF translocation inhibitor genistein and the specific V-ATPase inhibitor bafilomycin to dissect transcriptional pathways downstream of the (P)RR. In this dataset, we include the expression data obtained from KELLY cells incubated with genistein or bafilomycin A1. Five intervention samples and three control samples were analyzed. We generated the following pairwise comparisons using Chipinspector (Genomatix Software GmbH) and a FDR of 0.5% (bafilomycin), 5% (genistein): genistein- versus DMSO- and bafilomycin- versus DMSO-treated cells. ChipInspector carries out significance analysis on the single probe level. Normalized probe set level data not provided for individual Sample records. Processed data is available on Series record.

2013-07-05 | E-GEOD-39962 | biostudies-arrayexpress

Bulk RNA-seq of primary visceral adipocytes isolated from wildtype mice or mice with adipocyte specific deletion of Atg7

Project description:Genes involved in the autophagic pathway are risk factors for the development of inflammatory bowel disease. In addition, patients with Crohn’s disease exhibit a profound expansion of mesenteric fat during the pathology. We investigated in our study the role of autophagy in mature adipocyte during intestinal inflammation. Mice bearing a tamoxifen-inducible deletion of Atg7 specifically in adipocytes showed signs of exacerbated intestinal inflammation in response to DSS-induced colitis. We therefore aimed to understand the possible underlying reasons for this change and performed a bulk RNA-seq approach using primary visceral adipocytes.

2023-01-14 | E-MTAB-12498 | biostudies-arrayexpress

High Shear Stress Enhances Endothelial Permeability in the presence of a CAD Risk Locus

Project description:Single nucleotide polymorphisms are exceedingly common in non-coding loci, yet their impact on cellular dysfunction–especially under stressed conditions associated with coronary artery disease (CAD)–is still unclear. Here we show that when exposed to external stressors, the presence of polymorphisms in the non-coding 9p21.3 locus increases endothelial monolayer and microvessel dysfunction; endothelial cells (ECs) derived from induced pluripotent stem cells of patients homozygous for this risk haplotype (R/R WT) differentiated similarly to their non-risk (N/N) and isogenic knockout (R/R KO) counterparts; monolayers exhibited greater permeability and ROS signaling when the risk locus was present. Addition of the inflammatory cytokine TNFa further enhanced EC monolayer permeability but independent of risk haplotype. When wall shear stress was applied to ECs in a microfluidic vessel, R/R WT vessels were more permeable at lower shear stresses than R/R KO vessels. Transcriptomes of sheared cells clustered more by risk haplotype than by patient or clone, resulting in significant differential regulation of EC function and junction genes versus static conditions. A subset of previously identified CAD risk genes invert expression patterns in the presence of high shear concomitant with aberrant cell-cell adhesion, vessel permeability, and the risk haplotype, suggesting that shear stress could be a unique regulator of non-coding loci and its impact on CAD.

2021-06-08 | GSE167861 | GEO

Permeability

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Expression profiling of Noto-GFP+ notochord progenitor cells sorted from E8.5 mouse embryos

Project description:Using a combination of cell sorting and microarray analysis, we identified almost 200 genes as having a high level of expression in the notochord. After whole mount in situ hybridization screening, we confirmed approximately one third of these as having a novel notochord expression pattern. Keywords: cell type comparison - embryonic Noto-GFP+ notochord progenitors versus surrounding GFP- comparator cells 3 biological replicates - each replicate includes an experiment cell population (Noto-GFP positive cell sort) and a comparator population (GFP negative cell sort)

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Physiological Vascular Permeability Requires Induction of Endothelial NR4A1 by Progesterone Receptor

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-01-01 | E-GEOD-43789 | biostudies-arrayexpress

Analysis of muscular proteomics of deep pressure ulcers reveals JAK2 influence on muscle autophagy and apoptosis

Project description:Pressure ulcers (PU) is a complex and serious clinical problem. Deep tissue injury is either the outcome or the trigger of deep PU. However, the cellular and molecular mechanisms that contribute to the pathogenesis of deep PU remain unclear. In this study, the degeneration characteristics, increased autophagy and apoptosis were observed in deep PU muscle tissues by H&E staining, transmission electron microscope, TUNEL staining and western blot analysis. We further conducted quantitative liquid chromatography-tandem mass spectrometry analysis to explore the proteome of deep PU muscle, a total of 520 proteins were differently expressed, including 427 up-regulated and 93 down-regulated. In particular, downregulation was observed for Janus Kinase 2 (JAK2). Intriguingly, we showed that a distinctly reduced expression of JAK2 in C2C12 myoblasts exposed to oxygen-glucose deprivation and reoxygenation insult. Ex vivo, JAK2 overexpressed myoblasts exhibited decrease of autophagy and apoptosis with the same treatment, along with less cell death. Finally, western blot analysis determined that p-JAK2, p-PI3K, p-AKT, p-mTOR and p-ERK1/2 were significantly elevated, accompanied by JAK2 overexpression, but without p-STAT3. In conclusion, these results demonstrated that both autophagy and apoptosis involve in muscle damage of deep PU, and JAK2 may play an important protective role in muscular ischemia and reperfusion injury by activating AKT and ERK1/2 pathway to inhibit autophagy and apoptosis.

2019-11-12 | PXD009512 | Pride

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