Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Brain-to-cervical lymph node signaling after stroke

ABSTRACT: Microarray analysis of isolated lymphatic endothelial cells from cervical lymph nodes (CLNs) of ischemic mice showed the activation of transmembrane tyrosine kinase pathways.

ORGANISM(S): Mus musculus

PROVIDER: GSE138978 | GEO | 2019/10/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Brain-to-cervical lymph node signaling after stroke

Project description:Brain-to-cervical lymph node signaling after stroke

| PRJNA577918 | ENA

Meningeal lymphatic vasculature mediates cervical lymph node metastasis of brain tumors through VEGF-C/VEGFR3/eNOS signaling pathway

Project description:Purpose: The rediscovery of meningeal lymphatic vessels (MLVs) suggests a potential linkage between brain tumors and cervical lymph nodes (LNs). In this study, we investigated whether and how meningeal lymphatics regulate the metastasis of brain tumor cells. Experimental Design: We first examined the pattern of MLVs and LNs after tumor cells were injected into the cisterna magna (i.c.m.) or subdural space of mice. The meninges were isolated and analyzed by whole-mount immunofluorescence staining. LN metastasis was analyzed by detecting GFP+ tumor cells. Then we used inducible knock-out mice and AAV-VEGF-C delivery system to study the function of MLVs in mediating the metastasis of brain tumor cells. Finally, RNA-seq was used to determine the expression profiles of meningeal lymphatic endothelial cells (mLECs) in mice with or without tumors. The roles of the endothelial nitric oxide synthetase (eNOS) were evaluated both genetically and pharmacologically in vivo. Results: Meningeal lymphangiogenesis induced by GL261 and B16 tumors was correlated with dCLN swelling and metastasis. dCLN metastasis was suppressed in MLV-defective mice, while promoted in AAV-VEGF-C-treated mice. In addition, we found that VEGF-C/VEGFR3 signaling regulated both meningeal and tumor lymphangiogenesis. Tumor-associated mLECs have a distinct transcriptomic signature, which highly express eNOS. Furthermore, genetic or pharmacological inhibition of eNOS significantly suppressed meningeal lymphangiogenesis and dCLN metastasis. Conclusions: The meningeal lymphatic vasculature mediates the metastasis of brain tumors to cervical LNs, mainly through a VEGF-C/VEGFR3-eNOS signaling pathway, suggesting that MLV may be a potential therapeutic target for the extracranial metastasis of brain tumors.

2020-03-16 | GSE128207 | GEO

Transcription profiling of human early stage cervical cancer tumours WITH AND WITHOUT lymph node metastasis, IN ORDER TO predict lymph node metastasis BEFORE treatment.

Project description:Gene expression profiling of early stage cervical cancer tumours with and without lymph node metastasis, in order to predict lymph node metastasis before treatment. Subsequently, comparing gene expression profiles between healthy cervical tissue and early stage cervical cancer tissue. Experiment Overall Design: All patients had clinical FIGO stage IB-IIA cervical cancer, the low-risk group (N) included 19 patients without unfavourable prognostic factors (positive lymph nodes, parametrial invasion, positive margins or a combination of unfavourable prognostic factors); the high risk group (P) consisted of 16 patients with lymph node metastasis, who were treated with adjuvant radiation therapy with or without chemotherapy. Healthy cervical tissue biopsies (H) were collected from 5 non-cervical carcinoma patients who underwent hysterectomy for benign reasons. RNA pooled from all tumour tissue samples was used as reference sample. Log-ratios of five technical replicates were used for normalization.

2008-04-05 | E-GEOD-7410 | biostudies-arrayexpress

VEGF-C prophylaxis promotes lymphatic drainage, microglia modulation, and neuroprotection in response to stroke injury

Project description:Meningeal lymphatic vessels (MLVs) promote tissue clearance and immune surveillance in the central nervous system (CNS). Vascular endothelial growth factor-C (VEGF-C) regulates MLV development and maintenance and has therapeutic potential for treating neurological disorders. Herein, we investigated the effects of VEGF-C overexpression on brain fluid drainage and ischemic stroke outcomes in mice. Intra-cerebrospinal administration of an adeno-associated virus expressing mouse full-length VEGF-C (AAV-mVEGF-C) increased CSF drainage to the deep cervical lymph nodes (dCLNs) by enhancing lymphatic growth, and upregulated neuroprotective signaling pathways identified by single nuclei RNA sequencing of brain cells. In a mouse model of ischemic stroke, AAV-mVEGF-C pretreatment reduced stroke injury and ameliorated motor performances in the subacute stage, associated with mitigated microglia-mediated inflammation and increased BDNF signaling in brain cells. Neuroprotective effects of VEGF-C were lost upon ligation of the dCLN afferent lymphatics, and not mimicked by acute post-stroke VEGF-C injection. We conclude that VEGF-C prophylaxis promotes multiple vascular, immune, and neural responses that culminate in a protection against neurological damage in acute ischemic stroke.

2024-01-18 | GSE253051 | GEO

Human melanoma-derived extracellular vesicles reprogram dendritic cells potentially enabling lymph node metastases

Project description:Evolution of melanoma from a primary tumor to widespread metastasis is crucially dependent on lymphatic spread. The mechanisms regulating the initial step in metastatic dissemination via regional lymph nodes remain largely unknown. We have previously described a dysfunctional immune profile that precedes evidence of metastasis in the first node draining from the primary tumor, the sentinel lymph node (SLN). Herein, we explore the role of melanoma-derived extracellular vesicles (EVs) as mediators of this pre-metastatic niche through cargo-specific polarization of dendritic cells (DCs). Utilizing mass cytometry, pre-metastatic SLNs demonstrate compromised co-stimulatory CD80 expression compared to healthy lymph nodes. Similarly, DCs matured in vitro in the presence of melanoma EVs showed impaired co-stimulation and polarization towards a chronic inflammatory cytokine milieu. Profiling of melanoma EV cargo identified shared proteomic and RNA signatures including the signaling axis S100A8, S100A9 and cognate receptor TLR4. Mechanistically, S100A8 and S100A9 compromised DC maturation, a phenotype which was partially recovered following TLR4 blockade. Early evidence demonstrates similar EVs can be isolated from human afferent lymphatic fluid ex vivo. Taken together, we propose synergistic interactions among melanoma EV cargo are responsible for suppressing DC maturation, potentially explaining the survival of malignant melanocytes metastasizing into seemingly “normal” regional lymph nodes.

2018-10-26 | PXD005539 | Pride

Brain-to-cervical lymph node signaling after stroke.

Project description:After stroke, peripheral immune cells are activated and these systemic responses may amplify brain damage, but how the injured brain sends out signals to trigger systemic inflammation remains unclear. Here we show that a brain-to-cervical lymph node (CLN) pathway is involved. In rats subjected to focal cerebral ischemia, lymphatic endothelial cells proliferate and macrophages are rapidly activated in CLNs within 24 h, in part via VEGF-C/VEGFR3 signalling. Microarray analyses of isolated lymphatic endothelium from CLNs of ischemic mice confirm the activation of transmembrane tyrosine kinase pathways. Blockade of VEGFR3 reduces lymphatic endothelial activation, decreases pro-inflammatory macrophages, and reduces brain infarction. In vitro, VEGF-C/VEGFR3 signalling in lymphatic endothelial cells enhances inflammatory responses in co-cultured macrophages. Lastly, surgical removal of CLNs in mice significantly reduces infarction after focal cerebral ischemia. These findings suggest that modulating the brain-to-CLN pathway may offer therapeutic opportunities to ameliorate systemic inflammation and brain injury after stroke.

| S-EPMC6876639 | biostudies-literature

Differentially expressed genes in HSCC tissues, Normal hypopharyngeal tissue and Cervical lymph nodes

Project description:To identify differentially expressed genes by HSCC tissues, Normal hypopharyngeal tissues and Cervical lymph nodes were subjected to Agilent whole genome microarrays.

2021-07-18 | GSE180077 | GEO

Next Generation Sequencing identifies lymph node lymphatic endothelial cell genes regulated by RANKL

Project description:Purpose: The objective was to identify genes regulted by RANK signalling in lymph node lymphatic endothelial cells Method: Lymphatic endothelial cells were FACS sorted from peripheral lymph nodes of mice deficient for stromal RANKL (Ccl19 Cre Rankl flox/flox) versus littermate controls (Rankl flox/flox) and processed for bulk RNA sequencing Results: Upregulated and downregulated genes were identified

2019-06-01 | GSE129315 | GEO

transcriptome profile of CD200-deficient cervical lymph nodes and spleens

Project description:Comparative study between the cervical lymph nodes and spleens of C57BL/6 mice. The focus of our study was the examination of the transcriptome profiles in the lymphoid organs of C57BL/6 mice (wild type and CD200-deficient).

2011-11-24 | E-MEXP-2982 | biostudies-arrayexpress