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Transcription profiling of human dermal microvascular endothelial, fibroblast, and glioblastoma cells treated with mycophenolic acid

ABSTRACT: The effect of Mycophenolic acid on primary isolated human dermal microvascular endothelial (HDMVEC) and fibroblast cells as well as human glioblastoma brain tumor cell line (U87).

ORGANISM(S): Homo sapiens

SUBMITTER: Domhan S

PROVIDER: S-ECPF-TABM-315 | biostudies-other | 2008 Jun

REPOSITORIES: biostudies-other

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Transcription profiling of human dermal microvascular endothelial, fibroblast, and glioblastoma cells treated with mycophenolic acid

Project description:The effect of Mycophenolic acid on primary isolated human dermal microvascular endothelial (HDMVEC) and fibroblast cells as well as human glioblastoma brain tumor cell line (U87).

2008-06-25 | E-TABM-315 | biostudies-arrayexpress

Transcription profiling of human dermal endothelial cells treated with 10ng/ml VEGF and 20ng/ml basic Fibroblast Growth Factor (bFGF) for 6h

Project description:Cells were treated with 10ng/ml VEGF and 20ng/ml basic Fibroblast Growth Factor (bFGF) for 6h at 37°C with 5 % CO2 and 95 % humidity..

| S-ECPF-RZPD-14 | biostudies-other

Transcription profiling of irradiated human dermal microvascular endothelial cells

Project description:Human dermal microvascular endothelial cells (HDMVECs) were irradiated with 2 Gy or non-irradiated. Two methods of RNA isolation were used to comparatively analyze the miRNA status after radiation treatment.

2010-01-13 | E-TABM-617 | biostudies-arrayexpress

Sirtinol treatment reduces inflammation in human dermal microvascular endothelial cells.

Project description:Histone deacetylases (HDAC) are key enzymes in the epigenetic control of gene expression. Recently, inhibitors of class I and class II HDAC have been successfully employed for the treatment of different inflammatory diseases such as rheumatoid arthritis, colitis, airway inflammation and asthma. So far, little is known so far about a similar therapeutic effect of inhibitors specifically directed against sirtuins, the class III HDAC. In this study, we investigated the expression and localization of endogenous sirtuins in primary human dermal microvascular endothelial cells (HDMEC), a cell type playing a key role in the development and maintenance of skin inflammation. We then examined the biological activity of sirtinol, a specific sirtuin inhibitor, in HDMEC response to pro-inflammatory cytokines. We found that, even though sirtinol treatment alone affected only long-term cell proliferation, it diminishes HDMEC inflammatory responses to tumor necrosis factor (TNF)? and interleukin (IL)-1?. In fact, sirtinol significantly reduced membrane expression of adhesion molecules in TNFã- or IL-1?-stimulated cells, as well as the amount of CXCL10 and CCL2 released by HDMEC following TNF? treatment. Notably, sirtinol drastically decreased monocyte adhesion on activated HDMEC. Using selective inhibitors for Sirt1 and Sirt2, we showed a predominant involvement of Sirt1 inhibition in the modulation of adhesion molecule expression and monocyte adhesion on activated HDMEC. Finally, we demonstrated the in vivo expression of Sirt1 in the dermal vessels of normal and psoriatic skin. Altogether, these findings indicated that sirtuins may represent a promising therapeutic target for the treatment of inflammatory skin diseases characterized by a prominent microvessel involvement.

| S-EPMC3171404 | biostudies-literature

Expression data from BMP9-treated human dermal microvascular endothelial cells (HMVEC-D)

2012-09-19 | GSE40960 | GEO

Impact of Human Dermal Microvascular Endothelial Cells on Primary Dermal Fibroblasts in Response to Inflammatory Stress.

Project description:The aim of the present study was to evaluate the impact of the microenvironment produced by dermal microvascular endothelial cells, secondary to a pro-inflammatory challenge, on 2D culture models using dermal fibroblasts and in 3D reconstructed skin model using dermal fibroblasts and keratinocytes from healthy donors. We hypothesized that specific microvascular endothelial low grade inflammation could change fibroblasts phenotype and be involved in extracellular matrix (ECM) modification and skin alteration. Following IFNγ, TNFα, IL-1β pro-inflammatory stress on Human Dermal Endothelial Cells (HDMEC) we observed the increased release of Chemokine ligand 2 (CCL2), IL-6 and IL-8 but not VEGF-A in the conditioned medium (CM). The subsequent addition of this endothelial pro-inflammatory CM in dermal fibroblasts revealed an upregulation of IL6, IL8 and CCL2 but no NF-κB gene expression. The resulting ECM formation was impaired with a reduction of the collagen 1 network and a decrease in COL1A1 gene expression in 2D and 3D models. Collagen 1 and pro-LOX protein expression were significantly reduced confirming an impairment of the collagen network related to endothelial inflammation secretion. To conclude, this work showed that, without any immune cells, the endothelial secretion in response to a pro-inflammatory stress is able to activate the fibroblasts that will maintain the pro-inflammatory environment and exacerbate ECM degradation.

| S-EPMC6456658 | biostudies-literature

Inhibition of tRNA Gene Transcription by the Immunosuppressant Mycophenolic Acid.

Project description:Mycophenolic acid (MPA) is the active metabolite of mycophenolate mofetil, a drug that is widely used for immunosuppression in organ transplantation and autoimmune diseases, as well as anticancer chemotherapy. It inhibits IMP dehydrogenase, a rate-limiting enzyme in de novo synthesis of guanidine nucleotides. MPA treatment interferes with transcription elongation, resulting in a drastic reduction of pre-rRNA and pre-tRNA synthesis, the disruption of the nucleolus, and consequently cell cycle arrest. Here, we investigated the mechanism whereby MPA inhibits RNA polymerase III (Pol III) activity, in both yeast and mammalian cells. We show that MPA rapidly inhibits Pol III by depleting GTP. Although MPA treatment can activate p53, this is not required for Pol III transcriptional inhibition. The Pol III repressor MAF1 is also not responsible for inhibiting Pol III in response to MPA treatment. We show that upon MPA treatment, the levels of selected Pol III subunits decrease, but this is secondary to transcriptional inhibition. Chromatin immunoprecipitation (ChIP) experiments show that Pol III does not fully dissociate from tRNA genes in yeast treated with MPA, even though there is a sharp decrease in the levels of newly transcribed tRNAs. We propose that in yeast, GTP depletion may lead to Pol III stalling.

| S-EPMC6908259 | biostudies-literature

Scleroderma dermal microvascular endothelial cells exhibit defective response to pro-angiogenic chemokines.

Project description:ObjectivesAngiogenesis plays a critical role in SSc (scleroderma). The aim of this study was to examine the expression of growth-regulated protein-? (Gro-?/CXCL3), granulocyte chemotactic protein 2 (GCP-2/CXCL6) and their receptor CXCR2 in endothelial cells (ECs) isolated from SSc skin and determine whether these cells mount an angiogenic response towards pro-angiogenic chemokines. The downstream signalling pathways as well as the pro-angiogenic transcription factor inhibitor of DNA-binding protein 1 (Id-1) were also examined.MethodsSkin biopsies were obtained from patients with dcSSc. ECs were isolated via magnetic positive selection. Angiogenesis was measured by EC chemotaxis assay.ResultsGro-?/CXCL3 and GCP-2/CXCL6 were minimally expressed in both skin types but elevated in SSc serum. Pro-angiogenic chemokine mRNA was greater in SSc ECs than in normal ECs. SSc ECs did not migrate to vascular endothelial growth factor (VEGF), Gro-?/CXCL3, GCP-2/CXCL6 or CXCL16. The signalling pathways stimulated by these chemokines were also dysregulated. Id-1 mRNA in SSc ECs was lower compared with normal ECs, and overexpression of Id-1 in SSc ECs increased their ability to migrate towards VEGF and CXCL16.ConclusionOur results show that SSc ECs are unable to respond to pro-angiogenic chemokines despite their increased expression in serum and ECs. This might be due to the differences in the signalling pathways activated by these chemokines in normal vs SSc ECs. In addition, the lower expression of Id-1 also decreases the angiogenic response. The inability of pro-angiogenic chemokines to promote EC migration provides an additional mechanism for the impaired angiogenesis that characterizes SSc.

| S-EPMC5009475 | biostudies-literature

Expression data from BMP9-treated human dermal microvascular endothelial cells (HMVEC-D)

Project description:BMP9 signaling has been implicated in hereditary hemorrhagic telangiectasia and vascular remodeling, acting via the HHT target genes, endoglin and ALK1. This study sought to identify endothelial BMP9-regulated proteins that could affect the HHT phenotype. Gene ontology analysis of cDNA microarray data obtained following BMP9 treatment of primary human endothelial cells indicated regulation of chemokine, adhesion, and inflammation pathways. The sample set is comprised of three biological replicate control human dermal microvascular endothelial cells, and three treated (5 ng/ml human recombinant BMP9) biological replicate human dermal microvascular endothelial cells

2012-09-19 | E-GEOD-40960 | biostudies-arrayexpress

Transcription profiling of human dermal fibroblasts and lung microvascular endothelial cells irradiated with protons

Project description:Normal human dermal fibroblasts (NHDF) and human lung microvascular endothelial cells (HMVEC-L) were irradiated with protons (0, 0.5, 1 and 2 Gy, 1GEv/n) at Brookhaven National Labs (BNL). Aim of the study is to find differentially transcribed genes in dependence of radiation dose/source and cell type.

2009-04-25 | E-TABM-379 | biostudies-arrayexpress

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