Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA282531 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Afferent lymphatic vessels bring antigens and diverse populations of leukocytes to draining lymph nodes, but efferent lymphatics allow only lymphocytes to leave the nodes. Despite fundamental importance of afferent vs. efferent lymphatics in immune response and cancer spread, molecular characteristics of these different arms of the lymphatic vasculature are largely unknown. In this work we report marked transcriptional differences between afferent and efferent lymphatic endothelial cells. Mouse inguinal, axillary, and brachial lymphnodes were collected and cryomolds prepared for laser-capture microdissection. Frozen sections were stained with various cell marker antibodies and micro-dissection performed to collect lymphatic endothelial cells. Total RNA was extracted from the cells and used in microarray analysis. Alternatively, popliteal, caudal, lumbar, inguinal, mesenteric, renal, axillary, brachial, deep and superficial cervical LN were enzymatically digested, the cells stained, and FACs sorted before RNA isolation.
2016-08-24 | E-GEOD-68371 | biostudies-arrayexpress
Project description:Afferent lymphatic vessels bring antigens and diverse populations of leukocytes to draining lymph nodes, but efferent lymphatics allow only lymphocytes to leave the nodes. Despite fundamental importance of afferent vs. efferent lymphatics in immune response and cancer spread, molecular characteristics of these different arms of the lymphatic vasculature are largely unknown. In this work we report marked transcriptional differences between afferent and efferent lymphatic endothelial cells.
2016-08-24 | GSE68371 | GEO
Project description:Lymphatic vessels form a critical component in the regulation of human health and disease. While their functional significance is increasingly being recognized, the comprehensive heterogeneity of lymphatics remains uncharacterized. Here, we report the profiling of 33,000 lymphatic endothelial cells (LECs) in human lymph nodes (LNs) by single-cell RNA sequencing. Unbiased clustering revealed six major types of human LECs. LECs lining the sub-capsular sinus (SCS) of LNs abundantly expressed neutrophil chemoattractants, whereas LECs lining the medullary sinus (MS) expressed a C-type lectin CD209. Binding of a carbohydrate Lewis X (CD15) to CD209 mediated neutrophil binding to the MS. The neutrophil-selective homing by MS LECs may retain neutrophils in the LN medulla and allow lymph-borne pathogens to clear, preventing their spread through LNs in humans. Our study provides a comprehensive characterization of LEC heterogeneity and unveils a previously undefined role for medullary LECs in human immunity.
2019-08-08 | GSE124494 | GEO
Project description:Afferent lymphatic vessels (LVs) connect peripheral tissues with draining lymph nodes (dLNs) and are important for immune-surveillance and tissue drainage. They begin in the tissue as initial lymphatic capillaries, which are highly permeable and branched vessels specialized in the uptake of macromolecules, fluids and immune cells. Conversely, the downstream collecting LVs are impermeable and contractile structures that transport the taken up lymph and immune cells to the dLN. We and others have recently observed that intralymphatic leukocytes actively migrate within lymphatic capillaries but de-adhere and are passively transported by flow once they have reached in the collecting vessels. Besides potential differences in lymph flow we hypothesize that gene expression differences between capillaries and collectors could account for this transition from a crawling to a flowing mode of migration. In this project we aimed to perform a sequencing-based gene expression analysis of lymphatic endothelial cells (LECs) isolated from lymphatic capillaries and collectors, in order to identify new genes involved in leukocyte migration, as well as genes involved in shaping the morphologic phenotype of capillaries and collectors. For this, murine skin was enzymatically digested and LECs from capillaries or collectors were FACS-sorted and their RNA extracted and subjected to sequencing.
2021-05-07 | E-MTAB-9175 | biostudies-arrayexpress
Project description:<p>Breast cancer metastasis occurs via blood and lymphatic vessels. Breast cancer cells 'educate' lymphatic endothelial cells (LECs) to support tumor vascularization and growth. However, despite known metabolic alterations in breast cancer, it remains unclear how lymphatic endothelial cell metabolism is altered in the tumor microenvironment and its effect in lymphangiogenic signaling in LECs. We analyzed metabolites inside LECs in co-culture with MCF-7, MDA-MB-231, and SK-BR-3 breast cancer cell lines using 1H nuclear magnetic resonance (NMR) metabolomics, Seahorse, and the spatial distribution of metabolic co-enzymes using optical redox ratio imaging to describe breast cancer-LEC metabolic crosstalk. LECs co-cultured with breast cancer cells exhibited cell-line dependent altered metabolic profiles, including significant changes in lactate concentration in breast cancer co-culture. Cell metabolic phenotype analysis using Seahorse showed LECs in co-culture exhibited reduced mitochondrial respiration, increased reliance on glycolysis and reduced metabolic flexibility. Optical redox ratio measurements revealed reduced NAD(P)H levels in LECs potentially due to increased NAD(P)H utilization to maintain redox homeostasis. 13C-labeled glucose experiments did not reveal lactate shuttling into LECs from breast cancer cells, yet showed other 13C signals in LECs suggesting internalized metabolites and metabolic exchange between the two cell types. We also determined that breast cancer co-culture stimulated lymphangiogenic signaling in LECs, yet activation was not stimulated by lactate alone. Increased lymphangiogenic signaling suggests paracrine signaling between LECs and breast cancer cells which could have a pro-metastatic role.</p>
2024-06-25 | MTBLS859 | MetaboLights
Project description:Transcriptional profiling of mouse dural lymphatic endothelial cells (LECs) in comparing AAV-Controls with AAV-VEGFC treaded mice. Objective was to determine the effect of the VEGFC treatment on global gene expression of LECs.
2023-12-29 | GSE252115 | GEO
Project description:Human Notch1 intracellular domain (NICD) was overexpressed in human primary lymphatic endothelial cells (LECs) for 10 and 24 hours by adenovirus. A GFP-control adenovirus-infected cells (24hours) and uninfected cells were also analysed as controls. Total RNAs were harvested and subjected to Affymetrix U133A microarray. Human primary lymphatic endothelial cells (LECs) were isolated from human foreskin and cultured and expanded to population passages 5~6. Healthy subconfluent primary LECs were infected with adenovirus expressing human Notch1 intracellular domain (NICD) for 10 or 24 hours. In parallel, LECs were also infected with a GFP-expressing control adenovirus for 24 hours. Uninfected LECs were also used as a negative control in the same experiments
2010-03-20 | E-GEOD-20978 | biostudies-arrayexpress
Project description:In this analysis we have compared the gene expression profiles of lymphatic endothelial cells (LECs) isolated from human intestine (iLECs) versus LECs from human skin (dLECs).
2010-02-03 | E-MEXP-2452 | biostudies-arrayexpress
Project description:To observe the global changes in the lymphatic endothelial cells upon exposure to filarial antigens or parasites, LECs were stimulated for 24, 48, and 72hrs and the expression profiles were carried out. Human filarial parasites Brugia malayi and Wuchereria bancrofti habitat the lymphatics and cause lymphatic dilatation and lymphedema. In order to evaluate the effect of various stage specific effects on the lymphatic endothelial cells (LEC) and understand how they modulate the lymphatic dysfunction, LECs were stimulated in antigens derived from the Brugia malayi. These are preliminary time course data towards understanding how the filarial antigens induce lymphangiogenesis.
2010-05-19 | E-GEOD-15454 | biostudies-arrayexpress
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