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Dermal lymphatic endothelial cell response to type 2 diabetes [Homo sapiens]

ABSTRACT: 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 patientsÂ´ 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)

ORGANISM(S): Homo sapiens

SUBMITTER: Brigitte Hantusch

PROVIDER: E-GEOD-38396 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Dermal lymphatic endothelial cell response to type 2 diabetes [Homo sapiens]

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.

2012-06-02 | GSE38396 | GEO

Transcription profiling of human lymphatic endothelial cells, mouse dermal cells and human skin cells reveals an inflammation-induced mechanism for leukocyte transmigration of lymphatic vessel endothelium.

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

Dermal endothelial cells of type 2 diabetic patients

Project description:The prevalence of type 2 diabetes mellitus (T2D) is increasing constantly and various risk factors such as obesity, aging, nutritional states and physical inactivity, in addition to genetic pre-dispositions in different populations has been identified. The consequences of high blood glucose include damaged blood vessels, leading to arteriosclerosis and chronic diabetic microangiopathies. These changes lead to occlusive angiopathy, altered vascular permeability, or tissue hypoxia, resulting in complications such as heart disease, strokes, kidney disease, blindness, impaired wound healing, chronic skin ulcers, or amputations. We isolated dermal endothelial cells from diabetic patients (Pat) and control individuals (Ctrl) and performed RNASeq to compare differentially expressed genes.

2018-01-08 | GSE92724 | GEO

An inflammation-induced mechanism for leukocyte transmigration of lymphatic vessel endothelium.

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. Keywords: TNFalpha, Lymphatic endothelium, induction, Inflammation

2006-12-05 | GSE6257 | GEO

GNPS - Multi-omics analysis of endothelial cells reveals the metabolic diversity that underlies endothelial cell functions

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

Multi-omics analysis of endothelial cells reveals the metabolic diversity that underlies endothelial cell functions

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

Expression profile of human lymphatic endothelial cells under static or oscillatory shear stress conditions in the presence or absence of FOXC2

Project description:Lymphatic valves are specialized units regularly distributed along collecting vessels that allow unidirectional forward propulsion of the lymph, and its efficient transport from tissues to the bloodstream. Lymphatic endothelial cells that cover lymphatic valve sinuses are subjected to complex flow patterns, due to recirculation of the lymph during the collecting vessel pumping cycle. They also express high levels of FOXC2 transcription factor. We used microarrays to study the transcriptional networks controlled by FOXC2 in human lymphatic endothelial cells subjected to oscillatory shear stress or cultured under static conditions. Human lymphatic endothelial cells were transfected with control or FOXC2 siRNAs and subjected to 24-hour oscillatory shear stress (1 dyn/cm2; 1/4 Hz) or kept under static conditions as a control. RNA were amplified and hybridized on Affymetrix Human Gene 1.0 ST Arrays. The experiment was run twice independently, using each time a different siRNA to knockdown FOXC2, as previously described (Sabine et al, 2012, Dev Cell).

2015-11-09 | E-GEOD-60152 | biostudies-arrayexpress

Transcriptome analysis of endothelial cells of lymphatic vessel subtypes

Project description:To identify genes regulating the functional specification of collecting lymphatic vessels, we performed transcriptome profiling of dermal ECs isolated from adult mouse ear skin by flow cytometry.

2021-03-30 | GSE159842 | GEO

Lymphatic endothelial cells comparison gene array data

Project description:GeneChipÂ® 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 GeneChipÂ® 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 GeneChipÂ® Mouse Gene 2.0 ST Array. SVEC4-10 samples, human and mouse LEC samples.

2016-07-20 | E-GEOD-84551 | biostudies-arrayexpress

Novel protein interaction network of human calcitonin receptor-like receptor revealed by label-free quantitative proteomics

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

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