Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA150861 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptional profiling of TNF-M-NM-1 treated HUVECs comparing cells transfected microRNA negative control with cells transfected with miR-181b. Two-condition experiment, miR negative control VS. miR-181b transfected HUVECs. Biological replicates: 4 replicates of comparison of miR negative control VS. miR-181b
2012-05-15 | E-GEOD-35030 | biostudies-arrayexpress
Project description:Transcriptional profiling of TNF-α treated HUVECs comparing cells transfected microRNA negative control with cells transfected with miR-181b.
2012-05-16 | GSE35030 | GEO
Project description:The response of endothelial cells to diabetic-simulating stimuli is poorly understood. To evaluate the changes of enhancer activation status in HUVEC, genome-wide enrichment of H3K27ac (marker of enhancer and open chromatin) was examined in HUVECs treated with combined high glucose and TNF-alpha. HUVECs incubated in 25 mM mannitol were used as osmolarity control.
2023-02-08 | GSE205277 | GEO
Project description:Mice VSMCs: Control vs. TNF-α cultured
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Project description:In order to identify new markers of vascular cell senescence with potential in vivo implications, primary cultured Human Umbilical Vein Endothelial Cells (HUVECs), were analysed for microRNA (miR) expression. QRT-PCR microRNA expression profiling in 3 senescent (XIII passage) vs. 3 young HUVECs (II passage).
2012-05-15 | E-GEOD-37972 | biostudies-arrayexpress
Project description:Transcriptional profiling of mouse VSMCs comparing control with VSMCs cultured with TNF-α Apoptosis of vascular smooth muscle cells (VSMCs) is a process that regulates vessel remodeling in various cardiovascular diseases. The specific mechanisms that control VSMC apoptosis remain unclear. The present study aimed to investigate whether microRNA-494 (miR-494) is involved in regulating VSMC apoptosis and its underlying mechanisms. Cell death ELISA and terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assays were used to detect apoptosis of murine VSMCs following stimulation with tumor necrosis factor(TNF-α). The results indicated that TNF-α-upregulated VSMC apoptosis in a dose-dependent manner. Microarray analysis was used to evaluate the expression profile of microRNAs following TNF-α-stimulation in murine VSMCs. The expression of miR-494 was downregulated, whereas B-cell lymphoma 2-like 11 (BCL2L11) protein expression levels were upregulated in VSMCs following treatment with TNF- . Luciferase reporter assays confirmed that BCL2L11 was a direct target of miR-494. Transfection with miR-494 mimics decreased VSMC apoptosis and downregulated BCL2L11 protein levels. Conversely, transfection with miR-494 inhibitors increased cell apoptosis and upregulated BCL2L11 protein levels, suggesting that miR-494 may function as an essential regulator of BCL2L11. The increase in apoptosis caused by miR-494 inhibitors was abolished in cells co-transfected with BCL2L11-targeting small interfering RNA. The findings of the present study revealed that miR-494 inhibited TNF-α-induced VSMC apoptosis by downregulating the expression of BCL2L11.
2019-02-28 | GSE127016 | GEO
Project description:Effect of TNF-alpha on microRNAs levels in Human Umbilical Endothelial Cells (HUVECs). HUVEC that were treated or not for 2 or 24 hours with TNF (10 ng/ml). Duplicate samples (1 or 2) of two different isolations of HUVEC (A or B)
2009-12-01 | E-MTAB-150 | biostudies-arrayexpress
Project description:TNF alpha is one of the inflammatory mediator and induce genes mainly by transcriptional factor, p65, in endothelial cells. This time, we performed a time course study to detect the change of localization of p65 and Pol II. To identify p65 and Pol II binding sites, we used chromatin immunoprecipitation with deep sequencing (ChIP-seq) of HUVECs treated with or without TNF alpha for 30 mins. Cells were starved before stimulation longer than 16 hours. HUVECs were used within the first 6 passages. For crosslinking, 10 mM of EGS in 50% glacial acetic acid was used for 45 min, followed by 20 min of 1% paraformaldehyde treatmet was used.
2013-01-01 | E-GEOD-34500 | biostudies-arrayexpress
Project description:Macrophages are heterogeneous immune cells with distinct origins, phenotypes, functions and tissue localization. Their susceptibility to HIV-1 is subject to variations from permissiveness to resistance, owing in part to regulatory microRNAs. Here, we used RNAseq to examine the expression of >400 microRNAs in productively infected and bystander cells of HIV-1-exposed macrophage cultures. Two micro-RNAs up regulated in bystander macrophages, miR-221 and miR-222, were identified as negative regulators of CD4 expression and CD4-mediated HIV-1 entry. Both microRNAs were enhanced by TNF-α, an inhibitor of CD4 expression. MiR-221/miR-222 inhibitors recovered HIV-1 entry in TNF-α-treated macrophages by enhancing CD4 expression, and increased HIV-1 replication and spread in macrophages by countering TNF-α-enhanced miR-221/miR-222 expression in bystander cells. In line with these findings, HIV-1-resistant intestinal myeloid cells express higher levels of miR-221 than peripheral blood monocytes. Thus, miR-221/miR-222 act as effectors of the antiviral host response activated during macrophage infection that restrict HIV-1 entry.
2017-09-11 | GSE103394 | GEO
Project description:Purpose: Analyze the potential signaling pathways regulated by MLKL under TNF-induced endothelial cell inflammatory response Methods: HUVECs were allowed to grow to confluency and were starved with basal medium containing 0.5% FBS for 6h. Then treat HUVECs with vehicle, NSA, TNF-alpha, TNF-alpha+NSA for 6h and extract RNA. Results: NSA reduces the mRNA level of TNF-induced inflammation-related genes and most of these genes are downstream of NF-kappa B signaling pathway.
2020-01-04 | GSE142986 | GEO