Investigation of the gene expression profile of LYVE-1-positive macrophages
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE24492 | GEO | 2010/10/02
SECONDARY ACCESSION(S): PRJNA132529
REPOSITORIES: GEO
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Project description:LYVE-1-positive macrophages were observed to be closely spatially associated with the developing lymphatic vasculature. The role of this population of macrophages in the embryo is uncharacterised. We used microarray analyses to investigate which genes are differentially regulated between LYVE-1-positive and LYVE-1-negative macrophages Macrophage populations were isolated from cell suspensions prepared from digested embryonic day (E) 15.5 skin and prepared for RNA extraction and hybridization on Affymetrix microarrays.
2010-10-02 | E-GEOD-24492 | biostudies-arrayexpress
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Project description:Hyaluronan receptor LYVE-1 is expressed by liver sinusoidal endothelial cells (LSEC), lymphatic endothelial cells and specialized macrophages. Besides binding hyaluronan, LYVE-1 mediates adhesion of leukocytes and cancer cells to endothelial cells. Here, we analyzed the impact of LYVE-1 on physiological liver functions and metastasis. Mice with deficiency of Lyve-1 (Lyve-1 KO) were analyzed using histology, immunofluorescence, RNA sequencing, plasma proteomics and flow cytometry. Liver metastasis was studied by intrasplenic/intravenous injection of melanoma (B16F10luc2, WT31) or colorectal carcinoma (MC38) cell lines. Results: Hepatic architecture, liver size, endothelial differentiation and angiocrine functions were unaltered in Lyve-1 KO mice. Hyaluronan plasma levels were significantly increased in Lyve-1-KO mice; besides, plasma proteomics revealed increased carbonic anhydrase-2 and decreased FXIIIA, potential modulators of metastatis. Furthermore, gene expression analysis of LSEC indicated regulation of immunological pathways. Therefore, liver metastasis of a highly and of a weekly immunogenic tumor, i.e. melanoma and colorectal carcinoma (CRC), was analyzed in Lyve-1 KO mice. Hepatic metastasis of B16F10 luc2 and WT31 melanoma cells, but not MC38 CRC cells, was significantly reduced in Lyve-1 KO mice. While short-term adhesion assays with B16F10 luc2 cells in vivo did not show differences between Lyve-1 KO and wild-type mice, increased numbers of resident hepatic CD4+, CD8+ and regulatory T cells were detected in Lyve-1 KO livers. In addition, iron deposition was detected in F4/80+ liver macrophages known to exert pro-inflammatory effects. Conclusions: LYVE-1 deficiency controlled hepatic metastasis in a tumor cell-specific manner reducing hepatic metastasis of melanoma, but not CRC. Anti-tumorigenic effects are likely due to enhancement of the resident hepatic immune microenvironment.
2023-03-11 | PXD032717 | Pride
Project description:Beside their role in conventional immune regulation, macrophages are now recognised as essential regulator of local tissue homeostasis depending on the tissue in which they reside. Using phenotyping, we found that LYVE-1+ macrophages are the major resident macrophage population in murine aorta and adipose tissues under steady state. Furthermore, imaging analysis revealed the exclusive association of adipose tissue LYVE-1+ macrophages with smooth muscle positive large blood vessels. Hence, we hypothesize that LYVE-1+ macrophages sustain large vessel functional homeostasis. The present experiment aims to better characterize resident LYVE-1+ vs LYVE-1- macrophages in aorta and adipose tissues.
2018-06-01 | GSE114630 | GEO
Project description:Oncogenic mutations in PIK3CA, encoding p110α-PI3K, are a common cause of venous and lymphatic malformations. Vessel type-specific disease pathogenesis is poorly understood, hampering development of efficient therapies. Here, we reveal a new immune-interacting subtype of Ptx3-positive dermal lymphatic capillary endothelial cells (iLECs) that recruit pro-lymphangiogenic macrophages to promote progressive lymphatic overgrowth. Mouse model of Pik3caH1047R-driven vascular malformations showed that proliferation was induced in both venous and lymphatic ECs, but sustained selectively in LECs of advanced lesions. Single-cell transcriptomics identified the iLEC population, residing at lymphatic capillary terminals of normal vasculature, that was expanded in Pik3caH1047R mice. Expression of pro-inflammatory genes, including monocyte/macrophage chemokine Ccl2, in Pik3caH1047R-iLECs was associated with recruitment of VEGF-C-producing macrophages. Macrophage depletion, CCL2 blockade or anti-inflammatory COX-2 inhibition limited Pik3caH1047R-driven lymphangiogenesis. Thus, targeting the paracrine crosstalk between iLECs and macrophages provides a new therapeutic opportunity for lymphatic malformations. Identification of iLECs further indicates that peripheral lymphatic vessels not only respond to but also actively orchestrate inflammatory processes.
2023-01-16 | GSE201916 | GEO
Project description:Macrophages represent a heterogeneous myeloid population with diverse functions in normal tissues and tumors. While LYVE-1 macrophages have been identified in stromal regions of the normal mammary gland and mammary tumor, their functions in these regions remain unknown. Using a genetic LYVE-1+ macrophage deletion model, we demonstrate that loss of LYVE-1+ macrophages leads to accumulation of the extracellular matrix glycosaminoglycan hyaluronan. Consistent with this finding, we demonstrate that LYVE-1 expression correlates with an increased ability of macrophages to bind, internalize, and degrade hyaluronan. Furthermore, we demonstrate that deletion of LYVE-1+ macrophages results in increased hyaluronan accumulation in mammary tumors, which correlates with reduced tumor growth. Finally, using scRNA-seq, we demonstrate that deletion of LYVE-1 macrophages in tumors results in a shift in the remaining macrophages towards a pro-inflammatory phenotype. Together, these findings demonstrate that LYVE-1+ macrophages represent an anti-inflammatory macrophage population that contributes to tissue remodeling in the tumor microenvironment.
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Project description:Trafficking of leukocytes (dendritic cells, memory T cells, neutrophils) and tumor cells through the lymphatic network is a key process in inflammation and immunity and an important mechanism in metastatic spread of human cancers (1-3). Such trafficking involves both communication with and passage across lymphatic endothelium, the distinct endothelium that lines lymphatic vessels within the peripheral tissues and forms the lymphatic sinuses within lymph nodes. However, in comparison with blood vascular endothelium, there is only a rudimentary understanding of the molecular phenotype of lymphatic endothelium, and only a basic knowledge of the glycoconjugates that regulate leukocyte-endothelial and tumor cell-endothelial interactions in the lymphatic compartment. We would anticipate that changes in glycosylation of LEC cell surface proteins following activation might affect important functions associated withy LEC including eg. interactions with leukocytes and/or sequestration of GAG-binding chemokines. We already have shown that ligand binding to the lymphatic endothelial hyaluronan receptor LYVE-1 is reversibly masked by terminal sialation in LEC and that functional regulation of LYVE-1 is likely to be important in inflammation. An advantage of our proposal is that we can routinely isolate primary LEC in relatively large numbers, and have the necessary ethical approval to do so from human tissue. Glycan analysis of primary human lymphatic endothelial cells (LEC) in their resting and activated states, in normal and tumour tissues and a comparison of the LEC glycan structures with those from blood vessel endothelial cells
2011-06-14 | E-GEOD-29933 | biostudies-arrayexpress
Project description:ERG and FLI1 are important regulators of angiogenesis, but their role in lymphatic vasculature is less known. The goal of this study was to determine the role of ERG and FLI1 in postnatal lymphangiogenesis and their involvement in SSc lymphatic system defects. IF were used to detect ERG and FLI1 in SSc and healthy controls (HC) skin biopsies. Human lymphatic endothelial cells (LECs) were used in cell culture experiments. Transcriptional and chromatin analysis of ERG or FLI1 silenced LECs was performed using microarrays and ATAC-seq, respectively. Effects of ERG and FLI1 deficiency on in vitro tubulogenesis was examined using Matrigel assay. Erg and Fli1 endothelial specific knockouts (ErgCKO and Fli1CKO) and lymphatic specific knockouts (ProxErgCKO and ProxFli1CKO) were generated to examine vessel regeneration. ERG and FLI1 protein levels were reduced in blood and lymphatic vasculature in SSc skin biopsies. ERG and FLI1 were shown to regulate genes involved in lymphatic vessel specification, including VEGFR3/FLT4, LYVE-1, and PROX1, and this effect was, at least in part, due to chromatin remodeling. ERG/FLT4 pathway regulated in vitro tubulogenesis in LECs. Deficiency of Erg and Fli1 impaired function of blood and lymphatic vessel during wound healing. ERG and FLI1 are essential regulators of blood and lymphatic vessel regeneration. Deficiency of ERG and FLI1 in SSc endothelial cells, may contribute to rarefaction of blood and lymphatic vasculature in SSc patients. Microarray analysis was performed at The Boston University Microarray Core Facility. Affymetrix CEL files were normalized to produce gene-level expression values using the implementation of the Robust Multiarray Average (RMA) in the affy package (version 1.36.1) included within in the Bioconductor software suite (version 2.12) and an Entrez Gene-specific probe set mapping from BrainArray (version 16.0.0). RLE and NUSE quality metrics were computed using the affy PLM Bioconductor package (version 1.34.0). All microarray analyses were performed using the R environment for statistical computing (version 2.15.1).
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Project description:Investigation of the gene expression profile of LYVE-1-positive macrophages
| PRJNA132529 | ENA
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2019-11-12 | PXD013250 | Pride