Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA124481 | ENA |
REPOSITORIES: ENA
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Project description:Background : The G protein-coupled receptor (GPCR) calcitonin receptor-like receptor (CLR) is implicated in cardiovascular and skin diseases, migraine and cancer. Beyond its agonists, receptor activity-modifying proteins and receptor component protein, interacting partners of this GPCR (‘CLR interactome’) are currently unknown. Herein, we defined CLR interactome in primary human dermal lymphatic endothelial cells (HDLEC). Immunoprecipitation (IP) of core- and terminally-glycosylated CLR and label-free quantitative mass spectrometry allowed the identification of 46 novel interaction partners from a total HDLEC proteome consisting of 4,902 proteins. Aims: The main aim of this study was to characterise the interactome of endogenous CLR along with the expression of this GPCR in the context of the proteomic profile of primary human dermal lymphatic endothelial cells cultured in vitro. Methods We used label-free quantitative proteomic analysis to analyse the CLR co-IP eluates and total protein lysates obtained from cultured in vitro primary human dermal lymphatic endothelial cells (from Promocell).
2024-08-09 | PXD032156 | Pride
Project description:Analysis of ex vivo isolated lymphatic endothelial cells from the dermis of patients to define type 2 diabetes-induced changes. Results preveal aberrant dermal lymphangiogenesis and provide insight into its role in the pathogenesis of persistent skin inflammation in type 2 diabetes. The ex vivo dLEC transcriptome reveals a dramatic influence of the T2D environment on multiple molecular and cellular processes, mirroring the phenotypic changes seen in T2D affected skin. The positively and negatively correlated dLEC transcripts directly cohere to prolonged inflammatory periods and reduced infectious resistance of patients´ skin. Further, lymphatic vessels might be involved in tissue remodeling processes during T2D induced skin alterations associated with impaired wound healing and altered dermal architecture. Hence, dermal lymphatic vessels might be directly associated with T2D disease promotion. Global gene expression profile of normal dermal lymphatic endothelial cells (ndLECs) compared to dermal lymphatic endothelial cells derived from type 2 diabetic patients (dLECs).Quadruplicate biological samples were analyzed from human lymphatic endothelial cells (4 x diabetic; 4 x non-diabetic). subsets: 1 disease state set (dLECs), 1 control set (ndLECs)
2012-06-01 | E-GEOD-38396 | biostudies-arrayexpress
Project description:Intra- and extracellular metabolomics dataset of human dermal blood endothelial cells (HDBECs), human umbilical vein endothelial cells (HUVECs), human dermal lymphatic endothelial cells (HDLECs) and intestinal lymphatic endothelial cells (iLECs) in proliferation and quiescence.
2024-11-13 | MSV000096398 | GNPS
Project description:Untargeted proteomics dataset of human dermal blood endothelial cells (HDBECs), human umbilical vein endothelial cells (HUVECs), human dermal lymphatic endothelial cells (HDLECs) and intestinal lymphatic endothelial cells (iLECs) in proliferation and quiescence.
2024-11-13 | MSV000096399 | MassIVE
Project description:The exit of antigen-presenting cells (APC) and lymphocytes from inflamed skin to afferent lymph is vital for the initiation and maintenance of dermal immune responses. How such exit is achieved and how cells transmigrate the distinct endothelium of lymphatic vessels is however unknown. Here we show that inflammatory cytokines trigger activation of dermal lymphatic endothelial cells (LEC) leading to expression of the key leukocyte adhesion receptors ICAM-1, VCAM-1 and E-selectin, as well as a discrete panel of chemokines and other potential regulators of leukocyte transmigration. Furthermore, we show that both ICAM-1 and VCAM-1 are induced in the dermal lymphatic vessels of mice exposed to skin contact hypersensitivity where they mediate lymph node trafficking of DC via afferent lymphatics. Lastly, we show that TNF_-stimulates both DC adhesion and transmigration of dermal LEC monolayers in vitro and that the process is efficiently inhibited by ICAM-1 and VCAM-1 adhesion-blocking mAbs. These results reveal a CAM-mediated mechanism for recruiting leukocytes to the lymph nodes in inflammation and highlight the process of lymphatic transmigration as a potential new target for anti-inflammatory therapy. Experiment Overall Design: Global gene expression profile of normal dermal lymphatic endothelial cells cultured in media alone (no TNF) compared to that of normal dermal lymphatic endothelial cells stimulated with TNFalpha, 1 ng/ml for 48h.Triplicate biological samples were analyzed from human lymphatic endothelial cells (3 x controls; 3 x TNF treated) and a single sample analyzed from mouse lymphatic endothelial cells (1 x controls; 1 x TNF treated).
2008-11-07 | E-GEOD-6257 | biostudies-arrayexpress
Project description:GeneChip® Mouse Gene 2.0 ST Array for C57BL/6 mouse skin dermal primary lymphatic endothelial cells (Ms LEC) and mouse lymphatic endothelial cell line SVEC4-10 GeneChip® Human Gene 2.0 ST Array for human primary lymphatic endothelial cells (Hu LEC) Total RNA from lymphatic cell line SVEC4-10 were used for GeneChip® Mouse Gene 2.0 ST Array. SVEC4-10 samples, human and mouse LEC samples.
2016-07-20 | E-GEOD-84551 | biostudies-arrayexpress
Project description:GeneChip® Mouse Gene 2.0 ST Array for C57BL/6 mouse skin dermal primary lymphatic endothelial cells (Ms LEC) and mouse lymphatic endothelial cell line SVEC4-10 GeneChip® Human Gene 2.0 ST Array for human primary lymphatic endothelial cells (Hu LEC) Total RNA from lymphatic cell line SVEC4-10 were used for GeneChip® Mouse Gene 2.0 ST Array.
2016-07-20 | GSE84551 | GEO
Project description:Invasion of lymphatic vessels is a key step in the metastasis of primary tumour cells to draining lymph nodes. Recent evidence indicates that such metastasis can be facilitated by tumour lymphangiogenesis, although it remains unclear whether this is a consequence of increased lymphatic vessel numbers or alteration in the properties of the vessels themselves. Here we have addressed this important question by comparing the RNA profile of normal dermal lymphatic endothelial cells (LEC) with those isolated from tumours of murine T-241/VEGF-C metastatic fibrosarcoma. Our findings reveal significant changes in the expression of some 792 genes in tumour lymphatics (â?¥ 2 fold up/downregulation, p â?¤ 0.05), involving particularly transcripts associated with junctional adhesion, immunomodulation, extracellular matrix and vessel growth/patterning, several of which we have confirmed by RT-PCR and/or immunohistochemistry. Interestingly, this altered phenotype could not be attributed solely to VEGF-C induced lymphoproliferation, as no similar change in gene expression was reported when human LEC were cultured with VEGF-C in vitro. Moreover, we show that a key protein upregulated in the mouse model, namely the tight junction protein Endothelial Cell Specific Adhesion Molecule (ESAM), is similarly upregulated in tumour lymphatic vessels from 2/2 patients with head and neck squamous cell carcinoma and 4/4 patients with aggressive bladder carcinoma. These findings demonstrate a previously unrecognized influence of tumour environment on lymphatic gene expression and identify candidate tumour specific vessel markers that may prove valuable for either prognosis or therapy. Experiment Overall Design: Here we have investigated the invasion of lymphatic vessels as a key step in the metastasis of primary tumour cells to draining lymph nodes by comparing the gene expression profile of normal dermal lymphatic endothelial cells (LEC) with those isolated from tumours of murine T241/VEGF-C/GFP metastatic fibrosarcoma. Three biological replicates were analyzed from each group.
2008-10-25 | E-GEOD-6255 | biostudies-arrayexpress
Project description:During embryonic development, the lymphatic system emerges by transdifferentiation from the cardinal vein. Although lymphatic and blood vasculature share a close molecular and developmental relationship, they display distinct features and functions. However, even after terminal differentiation, transitions between the two endothelial cell types have been reported. Since changes in phenotypic plasticity and cellular differentiation processes frequently involve epigenetic mechanisms, we wondered whether DNA methylation might play a role in regulating cell type-specific expression in endothelial cells. By analyzing global gene expression and methylation patterns of primary human dermal lymphatic and blood endothelial cells, we identified a highly significant set of genes, which were differentially methylated and expressed. Pathway analyses of the differentially methylated and upregulated genes in lymphatic endothelial cells revealed involvement in developmental and transdifferentiation processes. We further identified a set of novel genes, which might be implicated in regulating BEC-LEC plasticity and could serve as therapeutic targets and/or biomarkers in vascular diseases associated with alterations in the endothelial phenotype. Expression profile of 10 lymphatic endothelial cells was compared to that of 6 blood endothelial cells, no replicates, no control samples.
2012-04-09 | E-GEOD-32709 | biostudies-arrayexpress
Project description:This study investigates the transcriptome of primary dermal lymphatic endothelial cells compared with blood vascular endothelial cells using samples isolated from wildtype embryos at defined points (E14.5, E16.5 and E18.5) during mouse embryonic development.
2022-11-21 | GSE184045 | GEO