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:Cancer metastasis into sentinel lymph nodes (LNs) is a crucial determinant of patient mortality. While it is recognized that tumor-induced lymphangiogenesis facilitates metastasis into LNs in murine models, the tumor-induced alterations in human lymphatic vessels remain obscure. Here we utilized single-cell RNA-seq to profile lymphatic endothelial cell (LEC) subsets in paired metastatic and non-metastatic LNs obtained from breast cancer patients. Tumor metastasis leads to a decrease in inflammatory LEC subsets such as subcapsular sinus LECs, while inducing increase of immunosuppressive CD200+ LECs. Matrix Gla protein (MGP) was the most upregulated gene in metastatic LN LECs, and its expression on LECs was VEGF and TGF-b dependent. Silencing MGP in LECs revealed that MGP promotes cancer cell adhesion to LECs. Thus, breast cancer cell metastasis into LNs remodels LEC subsets in human LNs and escalates MGP expression, which potentially facilitates the dissemination of cancer cells through lymphatics.
2025-09-01 | GSE248214 | 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:Cancer metastasis to sentinel lymph nodes (LNs) is often the first marker of potential disease progression. Although it is recognized that tumor-induced lymphangiogenesis facilitates metastasis into LNs in murine models, tumor-induced alterations in human lymphatic vessels remain obscure. We used single-cell RNA sequencing and high-resolution spatial transcriptomics to profile lymphatic endothelial cell (LEC) subsets in paired metastatic and non-metastatic LNs obtained from patients with treatment-naïve breast cancer. Tumor metastasis decreases immunoregulatory LEC subsets, such as PD-L1+ subcapsular sinus LECs, while inducing an increase in capillary-like CD200+ HEY1+ LECs. Matrix Gla protein (MGP) was the most upregulated gene in metastatic LN LECs, and its expression on LECs was TGF-b and VEGF dependent. Upregulated MGP promotes cancer cell adhesion to LN lymphatics. Thus, breast cancer cell metastasis to LNs remodels LEC subsets in human LNs and escalates MGP expression, potentially facilitating cancer cell dissemination through the lymphatic system.
2025-09-02 | GSE298872 | 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:Inflammatory responses are crucial in the pathological cardiac remodeling and repair after myocardial infarction (MI). The lymphatic endothelial cells (LECs) significantly influence immune cell clearance and mitigate cardiac inflammation. Chemokines are known to tightly regulate immune cell mobilization within the infarcted heart, thereby significantly influencing cardiac inflammation and remodeling. However, the role of chemokines expressed by LECs in the regulation of cardiac inflammation post-MI remains unclear. Our study revealed that the expression of CC chemokine CCL2 in cardiac LECs was sharply un-regulated following MI. We thus hypothesized that lymphatic endothelial CCL2 might be involved in post-MI cardiac remodeling. To test this hypothesis, we generated LEC-conditional Ccl2 knock-out mice. In vivo experiments demonstrated that the LEC-Ccl2 deficiency deteriorated cardiac function and worsened adverse cardiac remodeling after MI. Further analysis showed that the loss of CCL2 in LECs impeded post-MI lymphangiogenesis and increased macrophage infiltration in post-MI myocardium and impaired macrophages clearance via afferent cardiac lymphatics. This led to exacerbated inflammatory responses and pathological cardiac remodeling after MI. Mechanistically, our study identified that LECs expressed and secreted CCL2, which played a dual role. LEC-CCL2 recruit macrophages from the infarcted myocardium into the lymphatic system and activated AKT/ETS1 signaling, enhancing VEGFC expression and promoting lymphangiogenesis in an autocrine manner. This study reveals that cardiac LEC-expressing CCL2 tightly control macrophage trafficking via lymphatic vessels in injured hearts and thus diminished post-MI inflammatory responses and lessened adverse cardiac remodeling. This study demonstrates that CCL2 expression in cardiac LECs tightly controls macrophage trafficking via lymphatic vessels in injured hearts, thereby diminishing post-MI inflammatory responses and lessening adverse cardiac remodeling. This study suggests that modulating CCL2 signaling in LECs could provide a promising therapeutic target for resolving excessive inflammation and ameliorating adverse cardiac remodeling after MI.
2026-02-25 | GSE275188 | GEO
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