Expression data from interleukin-stimulated HUVEC
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE22325 | GEO | 2011/07/01
SECONDARY ACCESSION(S): PRJNA127523
REPOSITORIES: GEO
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Project description:In the hematopoietic microenvironment, endothelial cells (ECs) play an important role in the regulation of hematopoietic cell proliferation and trafficking. We previously demonstrated that EC stimulated with tumor necrosis factor alpha (TNF-α) induce the generation of dendritic cells from CD34(+) stem cells, whereas in contrast, interleukins were capable of inducing the proliferation of hematopoietic and myeloid progenitors. In order to identify potentially new soluble factors which greatly impact the self-renewal, proliferation and differentiation of CD34+ hematopoietic stem cells (HSC), we examined the expression profiles of IL-1ß, IL-3 and IL-6 stimulated human umbilical vein endothelial cells (HUVEC). we processed seven different umbilical cords and isolated 129 samples for total RNA, and pooled them into 18 groups corresponding to each stimulant, control and time point.
2011-07-01 | E-GEOD-22325 | biostudies-arrayexpress
Project description:Complete identification of the bone marrow niche remains one of the most progressing fields. Attempts to identify soluble factors involved in stem cell renewal have been less successful. We have previously shown that endothelial cells (EC) can induce the long-term proliferation of hematopoietic progenitor cells (HPC), especially when they had been subjected to an inflammatory stimulus like interleukins (IL) 1. To identify yet unknown growth factors, we compared the expression profile of IL-1 stimulated and non-stimulated endothelial cells. Human endothelial cells were subjected to IL-1 for 4, 8, and 16 hours. Isolated mRNA was analyzed by oligonucleotide microarray chips covering over 46,000 human genes.
2010-07-30 | E-GEOD-19240 | biostudies-arrayexpress
Project description:Complete identification of the bone marrow niche remains one of the most progressing fields. Attempts to identify soluble factors involved in stem cell renewal have been less successful. We have previously shown that endothelial cells (EC) can induce the long-term proliferation of hematopoietic progenitor cells (HPC), especially when they had been subjected to an inflammatory stimulus like interleukins (IL) 1. To identify yet unknown growth factors, we compared the expression profile of IL-1 stimulated and non-stimulated endothelial cells.
2010-07-01 | GSE19240 | GEO
Project description:EXPERIMENT: Microarray expression profiles derived from the human primary gingival epithelial cells 24.0h after exposure to heat inactivated P. gingivalis ANIMAL MODEL: NON EXPOSURE: Human primary gingival epithelial cells (at 3rd passage) were exposed to heat inactivated P. gingivalis (MOI:100) at 90% confluence. Two types of gingival epithelial cells were used. One with Normal cytokine inducer type (at least 2 fold IL-6/TNF-alpha/IL-1ß when challenged with TLR2/4 agonists) and the other with diminished cytokine inducer type (no change in IL-6/TNF-alpha/IL-1ß when challenged with TLR2/4 agonists). INTERVAL: NON. PLATFORM: microRNA expression profile in gingival epithelial cells - miRCURY LNA™ microRNA Arrays (Exiqon). The RNA samples were subjected to microarray on 8/9/2007 Keywords = Human primary gingival epithelial cells Keywords = P. gingivalis Keywords = Periodontitis Keywords: Ordered
2008-11-07 | GSE13042 | GEO
Project description:The systemic inflammatory response syndrome (SIRS) is a life-threatening medical condition characterized by a severe and generalized inflammatory state that can lead to multiple organ failure and shock. The central nervous system (CNS) regulates many features of SIRS, such as fever, cardiovascular and neuroendocrine responses. <br> <br> Central and systemic manifestations of SIRS can be induced by LPS or interleukin-1ß (IL-1ß) administration. The crucial role of IL-1ß in inflammation has been further highlighted by studies of mice lacking caspase 1 (casp1, also known as IL-1ß convertase), a protease that cleaves pro-IL-1ß into mature IL-1ß. Indeed, casp1 knockout (casp1-/-) mice survive lethal doses of LPS. The key role of IL-1ß in sickness behavior and its de-novo expression in the CNS during inflammation led us to test the hypothesis that IL-1ß plays a major role modulating the brain transcriptome during SIRS. <br> <br> We show here a genetic background environment effect caused by LPS administration in casp1-/- when compared to wild-type mice affecting the expression several genes, such as chemokines, GTPases, the metalloprotease ADAMTS1, IL-1RA, the inducible nitric oxide synthase (NOS2) and cyclooxygenase-2 (COX-2) were differentially increased by. Our findings may contribute to the understanding of the molecular changes that take place within the CNS during sepsis and SIRS and the development of new therapies for these serious conditions. Our results indicate that those genes may also play a role in several neuropsychiatric conditions in which inflammation has been implicated, and indicate that casp1 might be a potential therapeutic target for such disorders.
2008-03-02 | E-MEXP-1017 | biostudies-arrayexpress
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2010-10-26 | GSE16745 | GEO
Project description:Reintroduction of CEBPA in MN1-overexpressing hematopoietic cells prevents their hyper-proliferation and restores myeloid differentiation. Forced expression of MN1 in primitive mouse hematopoietic cells causes acute myeloid leukemia and impairs all-trans retinoic acid (ATRA) induced granulocytic differentiation. Here, we studied the effects of MN1 on myeloid differentiation and proliferation using primary human CD34+ hematopoietic cells, lineage depleted mouse bone marrow cells, and bipotential (granulocytic/monocytic) human AML-cell lines. We show that exogenous MN1 stimulated the growth of CD34+ cells, which was accompanied by enhanced survival and increased cell cycle traverse in cultures supporting progenitor cell growth. Forced MN1 expression impaired both granulocytic and monocytic differentiation in vitro in primary hematopoietic cells and AML cell lines. Endogenous MN1 expression was higher in human CD34+ cells compared to both primary and in vitro differentiated monocytes and granulocytes. Microarray and real time RT-PCR analysis of MN1-overexpressing CD34+ cells showed down regulation of CEBPA and its downstream target genes. Re-introduction of conditional and constitutive CEBPA overcame the effects of MN1 on myeloid differentiation and inhibited MN1-induced proliferation in vitro. These results indicate that down regulation of CEBPA activity contributes to MN1-modulated proliferation and impaired myeloid differentiation of hematopoietic cells Human BM derived CD34+ cells (Stemcell Technologies, Vancouver, BC, Canada) were expanded for 2 days and transduced with MSCV-IRES-GFP or MSCV-MN1-IRES-GFP retrovirus for another 2 days. One day later RNA was isolated from GFP+/CD34+ FACS-sorted cells using Trizol (Sigma) and samples were subjected to micro array analysis following Affymetrix protocols (Affymetrix, Santa Clara, CA) using the GeneChip Human U133 Plus 2.0 array
2010-10-26 | E-GEOD-16745 | biostudies-arrayexpress
Project description:Endothelial cells cover the lining of different blood vessels and lymph nodes, and have major functions including the transport of blood, homeostasis, inflammatory responses, control of infiltration of circulating cells into the tissues, and formation of new blood vessels. Therefore, understanding these cells is of major interest. The morphological features, phenotype and function of endothelial cells varies according to the vascular bed examined. The sialomucin, CD34, is widely used as an endothelial marker. However, CD34 is differentially expressed on endothelial cells in different organs and in pathological conditions. Little is known about regulation of endothelial CD34 expression or function. This marker is also strongly modified in-vitro in endothelial cell models, including human umbilical vein endothelial cells (HUVEC) and endothelial progenitor cells (EPC). We have therefore selected CD34high and CD34low endothelial cell subpopulations and examined their CD34 expression and function. Results: Transcriptomic analysis showed that CD34 gene and protein expressions are highly correlated, that CD34high cells are less proliferative, and have a stronger expression of IL-33 and Angiopoietin 2, compared to CD34low cells. Higher secretion levels of IL-33 by CD34high HUVECs was confirmed by ELISA. Finally, when endothelial cells were allowed to interact with peripheral blood mononuclear cells (PBMCs), CD34high endothelial cells induced a stronger proliferation of regulatory T lymphocytes (Tregs) compared to CD34low cells whereas expansion of other CD4+-T cell subsets was equivalent. These results suggest that CD34 expression by endothelial cells in-vitro associates with their ability to proliferate and with an immunogenic ability that favours the tolerogenic response.
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