Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

12 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data of blood (BVEC) versus lymphatic (LVEC) vascular endothelial silenced for RhoB and VEZF1

ABSTRACT: RhoB null mice show decreases in pathological angiogenesis in the ischemic retina and reduces angiogenesis in response to cutaneous wounding, but enhances lymphangiogenesis following both dermal wounding and inflammatory challenge. We used microarrays to link these unique and opposing roles of RhoB in blood versus lymphatic vasculatures to RhoB/VEZF1-mediated gene regulation in primary human blood versus lymphatic endothelial cells. Pure populations of human primary BVECs and LVECs silenced for RhoB or VEZF1 were used for RNA extraction and hybridization on Affymetrix microarrays. We extracted these cells from human male foreskins from at least four individuals and purified them using Dynabeads associated with vascular markers (CD31 and Podoplanin).

ORGANISM(S): Homo sapiens

SUBMITTER: Sharon Shechter

PROVIDER: E-GEOD-51754 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression data of blood (BVEC) versus lymphatic (LVEC) vascular endothelial silenced for RhoB and VEZF1

Project description:RhoB null mice show decreases in pathological angiogenesis in the ischemic retina and reduces angiogenesis in response to cutaneous wounding, but enhances lymphangiogenesis following both dermal wounding and inflammatory challenge. We used microarrays to link these unique and opposing roles of RhoB in blood versus lymphatic vasculatures to RhoB/VEZF1-mediated gene regulation in primary human blood versus lymphatic endothelial cells.

2013-10-28 | GSE51754 | GEO

RNA-seq analysis of control and podoplanin knockdown lymphatic endothelial cells

Project description:To determine the transcriptome changes after podoplanin was knocked down in human lymphatic endothelial cells Human lymphatic endothelial cells were transfected with control siRNA and podoplanin siRNA (N=2 for each group). After 48 hours, total RNA was isolated and processed for RNA-seq.

2016-03-14 | E-GEOD-79160 | biostudies-arrayexpress

Transcription profiling of lymphatic endothelial cell subtypes expressing high and low levels of podoplanin

Project description:We microprepared native mammary skin resections from healthy female donors (breast size reduction) by a combination of enzymatic and mechanical treatment. The resulting suspensions of single dermal cells were then subjected to FACSorting using antibodies against the lymphovascular marker protein podoplanin and the panendothelial protein CD31 as positive and the leukocytic protein CD45 as negative markers. We aimed at separating lymphatic vascular endothelial cells (LECs) from blood vascular endothelial cells (BECs) in order to characterize their moelcular and functional phenotypes in health and disease. We found that lymphatic endothelial cells consisted of two instead of only one cell population. Their discrimination marker was high versus low expression of podoplanin surface protein, respectively. Especially, the low-podoplanin expressors were undescribed. Thus, we screened for their transcription profile using U133A. We identified specific marker genes and finally have assigned a specific function to the novel LEC subpopulation unknown up to now. Importantly, we did not use lysates from cell culture, but from ex vivo cells. Thus, there was no treatment of cells except processing the samples on ice.

2007-07-01 | E-TABM-227 | biostudies-arrayexpress

Nicotinic acetylcholine receptors and EGF induce c-Kit ligand/Stem Cell Factor (SCF) in a M-NM-2-arrestin-1 and E2F1 dependent manner in NSCLC

Project description:Lung cancer remains the leading cause of cancer-related deaths worldwide. M-NM-2-arrestin-1 (ARRB1), a scaffolding protein involved in the termination or desensitization of signals arising from activated G-protein-coupled receptors (GPCRs) has been shown to play a role in invasion and proliferation of many cancers, including nicotine-induced proliferation of human nonM-bM-^@M-^Ssmall cell lung cancers (NSCLCs). In this study, we analyzed nicotine induced and M-NM-2-arrestin-1 dependent genes from the microarray data. Our analysis show that SCF (Stem cell factor) strongly differentiated smokers from non-smokers implying an important role of this gene in NSCLCs. SCF, a major cytokine is the ligand for the c-Kit proto-oncogene. Here we elucidate the molecular mechanisms by which nicotine as well as EGF induces the expression of SCF in lung adenocarcinoma cell lines A549 and H1650. ChIP assays and transient transfection experiments showed that transcription factor E2F1 can positively regulate SCF expression at the transcriptional level; depletion of E2F1 or M-NM-2-arrestin-1 prevented the nicotine-mediated induction of SCF. Given that the binding of SCF to c-Kit leads to activation of multiple downstream signaling pathways including Src, PI3K, MEK and EGFR pathways, our data suggest that the SCF plays a central role in lung carcinogenesis, and may be a potential therapeutic target for combating NSCLC. Studies presented here also provide evidence that SCF along with nicotine promotes self-renewal and proliferation of lung cancer stem cells (CSCs). Our findings reveal an important role and prognostic significance of SCF that can serve as a novel prognostic and predictive biomarker for NSCLC. Transfection of A549 cell line with control siRNA, Beta arrestin siRNA and then stimulation of nicotine

2013-11-10 | E-GEOD-44617 | biostudies-arrayexpress

RNA sequencing analysis of IECs from WT and RhoB-/- mice

Project description:Purpose: RhoB regulates cell functions, such as vesicular transport, apoptosis, autophagy, DNA repair, angiogenesis, proliferation, migration and invasion. We investigated whether RhoB is involved in the pathogenesis of ulcerative colitis (UC).We performed RNA sequencing analysis in intestinal epithelial cells (IECs) from RhoB-deficient mice and WT mice to study the molecular mechanisms through which RhoB regulates goblet cell numbers and epithelial regeneration and confirmed findings in colonic organoids from RhoB-deficient mice and WT mice and siRhoB transfected SW480 cells.

2022-09-27 | GSE170994 | GEO

RNA-seq analysis of control and podoplanin knockdown lymphatic endothelial cells

Project description:To determine the transcriptome changes after podoplanin was knocked down in human lymphatic endothelial cells

2016-03-14 | GSE79160 | GEO

Angiogenesis in the skin of SHARPIN-deficient mice with chronic proliferative dermatitis

Project description:Angiogenesis is a common feature of pathological processes including wound healing, tumor formation, and chronic inflammation. Chronic inflammation can also be associated with dilation or proliferation of lymph vessels. We examined blood vessels and lymphatics and the expression of pro- and anti-angiogenic genes in the skin of SHARPIN-deficient mice which spontaneously develop a chronic proliferative dermatitis (cpdm). The number of blood vessels in the dermis of cpdm mice increased with age as the inflammation progressed. Lymphatics identified by labeling for LYVE1 and podoplanin were moderately dilated, but they were not increased in number. The expression of proangiogenic Vegfa, Flt1 and anti-angiogenic Sema3a mRNA was increased. VEGFA was primarily localized in keratinocytes of cpdm skin. There was also increased expression of Ece1 and Pdpn mRNA. Podoplanin was restricted to lymphatic endothelial cells in normal skin, but fibroblasts in cpdm skin also reacted with anti-podoplanin antibodies indicating that they were activated. The expression of other angiogenic and lymphangiogenic factors was not altered or decreased. These results indicate that cpdm mice may be a useful model to study the pathogenesis of angiogenesis in chronic inflammation.

2016-05-21 | GSE81683 | GEO

Expression signatures of the lipid-based Akt inhibitors phosphatidylinositol ether lipid analogues in NSCLC cells

Project description:Activation of the serine/threonine kinase Akt contributes to the formation, maintenance, and therapeutic resistance of cancer, which is driving development of compounds that inhibit Akt. Phosphatidylinositol ether lipid analogues (PIAs) are analogues of the products of PI3K that inhibit Akt activation, translocation, and the proliferation of a broad spectrum of cancer cell types. To gain insight into the mechanism of PIAs, time-dependent transcriptional profiling of 5 active PIAs and the PI3K inhibitor LY294002 (LY) was performed in non-small cell lung cancer (NSCLC) cells using high-density oligonucleotide arrays. Gene ontology analysis revealed genes involved in apoptosis, wounding response, and angiogenesis were upregulated by PIAs, while genes involved in DNA replication, repair and mitosis were suppressed. Genes that exhibited early differential expression were partitioned into 3 groups; those induced by PIAs only (DUSP1, KLF6, CENTD2, BHLHB2, PREX1), those commonly induced by PIAs and LY (TRIB1, KLF2, RHOB and CDKN1A), and those commonly suppressed by PIAs and LY (IGFBP3, PCNA, PRIM1, MCM3 and HSPA1B). Increased expression of the tumor suppressors RHOB (RhoB), KLF6 (COPEB) and CDKN1A (p21Cip1/Waf1) was validated as an Akt-independent effect that contributed to PIA-induced cytotoxicity. Despite some overlap with LY, active PIAs have a distinct expression signature that contributes to their enhanced cytotoxicity.

2011-03-23 | GSE27911 | GEO

Transcriptional profiling of immortalized LECs (imLECs)

Project description:In contrast to the migration of leukocytes from blood vessels into tissues, and the involvement of adhesion molecules and chemokines in this process, the migration of leukocytes from the tissue into lymphatic vessels is much less well understood. This can, in part be explained by the fact that murine lymphatic endothelial cells (LECs) have proven particularly hard to isolate and propagate in culture. Hence, it has been difficult to establish suitable models to study this process in vitro. Combining magnetic bead-based purification and fluorescence-activated cell sorting (FACS), we have isolated LECs (immorto-LECs) from the skin of mice which express a temperature-sensitive SV40 large T antigen (H-2Kb-tsA58 mice; ImmortoMice) in all cell types under the control of the MHC-class-I-promotor, H-2Kb. The isolated cells are viable for more than 30 passages when cultured at 33 M-BM-:C, the temperature at which the large T antigen is stably expressed. Furthermore, immorto-LECs tolerate several days of culture at 37 M-BM-:C, but become senescent if continuously cultured at this temperature. All cells stably express endothelial and lymphatic markers like CD31, podoplanin, Prox-1 and VEGFR-3 up to passage 30. When cultured in presence of tumor necrosis factor-alpha (TNF-a), immorto-LECs upregulate adhesion molecules, such as ICAM-1, VCAM-1 and E-selectin, similarly to what has been reported to occur under inflammatory conditions in vivo. Overall, our findings establish immorto-LECs as a useful and handy tool for the in vitro investigation of immune cell transmigration across lymphatic endothelium. imLEC were cultured at 33 M-BM-:C until they reached approx. 70% confluence. Cells were then transferred to 37 M-BM-:C and cultured for 3 days in order to induce T antigen degradation. RNA was isolated from 3 different cultures of passages 13, 14 and 18

2011-03-31 | E-GEOD-28234 | biostudies-arrayexpress

Bulk RNA-Sequencing of mouse large intestinal lymphatics (capillaries and collectors)

Project description:Purpose: Profile global gene expression of intestinal lymphatics to compare with published datasets Methods: Intestinal tissues were digested, lymphatic endothelial cells were sorted using lymphatic markers including CD31, Podoplanin, Lyve1. Total RNA was isolated from sorted cells using the Direct-Zol RNA MiniPrep kit (Zymo). Samples were submitted for bulk RNA-Sequencing. Conclusions: Gobal gene expression profile of intestinal lymphatics for further comparison with published datasets

2022-06-21 | GSE199082 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data