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SMAD1/5 binding regions and expression data of human umbilical vein endothelial cells (HUVECs) and pulmonary arterial smooth muscle cells (PASMCs) treated with BMPs

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

OTHER RELATED OMICS DATASETS IN: PRJNA143113PRJNA138481PRJNA143115PRJNA141765PRJNA141767

ORGANISM(S): Homo sapiens

PROVIDER: GSE27661 | GEO | 2011/07/16

SECONDARY ACCESSION(S): PRJNA138481

REPOSITORIES: GEO

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SMAD1/5 binding regions of human pulmonary arterial smooth muscle cells (PASMCs) treated with BMP

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Curcuminoids Inhibit Angiogenic Behaviors of Human Umbilical Vein Endothelial Cells via Endoglin/Smad1 Signaling.

Project description:Angiogenesis is primarily attributed to the excessive proliferation and migration of endothelial cells. Targeting the vascular endothelial growth factor (VEGF) is therefore significant in anti-angiogenic therapy. Although these treatments have not reached clinical expectations, the upregulation of alternative angiogenic pathways (endoglin/Smad1) may play a critical role in drug (VEGF-neutralizing agents) resistance. Enhanced endoglin expression following a VEGF-neutralizing therapy (semaxanib®) was noted in patients. Treatment with an endoglin-targeting antibody augmented VEGF expression in human umbilical vein endothelial cells (HUVECs). Therefore, approaches that inhibit both the androgen and VEGF pathways enhance the HUVECs cytotoxicity and reverse semaxanib resistance. The purpose of this study was to find natural-occurring compounds that inhibited the endoglin-targeting pathway. Curcuminoids targeting endoglin were recognized from two thousand compounds in the Traditional Chinese Medicine Database@Taiwan (TCM Database@Taiwan) using Discovery Studio 4.5. Our results, obtained using cytotoxicity, migration/invasion, and flow cytometry assays, showed that curcumin (Cur) and demethoxycurcumin (DMC) reduced angiogenesis. In addition, Cur and DMC downregulated endoglin/pSmad1 phosphorylation. The study first showed that Cur and DMC demonstrated antiangiogenic activity via the inhibition of endoglin/Smad1 signaling. Synergistic effects of curcuminoids (i.e., curcumin and DMC) and semaxanib on HUVECs were found. This might be attributed to endoglin/pSmad1 downregulation in HUVECs. Combination treatment with curcuminoids and a semaxanib is therefore expected to reverse semaxanib resistance.

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Primary human umbilical vein and arterial endothelial cells

Project description:Human umbilical cords were obtained from the Lucille Packard Children Hospital. In this study, we devised a rapid isolation scheme to preserve the in vivo phenotype of each endothelial subtype. ECs were first isolated from umbilical cords by collagenase perfusion through the vein or artery as described. Cells were further purified using a Percoll density gradient (Amersham Biosciences, Piscataway, NJ) to remove residual erythrocytes and platelets. 1-5 x 106 ECs were then cultured overnight on gelatin-coated T12.5 flasks in Clonetics EGM-2 media (Cambrex Bio Science, Walkersville, MD) in which the ECs generally reached confluence the next morning. The confluent EC were trypsinized and subjected to two rounds of immuno-magnetic beads purification, adapted from a published purification protocol. There was a negative selection step using CD14, CD45 and CD64 to remove residual contaminating leukocytes, followed by positive selection using a mouse anti-endothelial cell monoclonal antibody (anti-CD146/clone P1H12 purchased from Chemicon, Temecula, CA). Total processing time was limited to 20 to 24 hours. The homogeneous, viable, primary ECs were used immediately to construct the library. The construction of SAGE libraries was performed with the I-SAGE kit (Invitrogen, Carlsbad, CA) per manufacturer’s instructions Keywords: other

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Primary human umbilical vein and arterial endothelial cells

2009-12-30 | E-GEOD-1539 | biostudies-arrayexpress

Human umbilical vein endothelial cells (HUVECs) treated with fenofibrate

Project description:This SuperSeries is composed of the SubSeries listed below.

2009-08-24 | GSE15494 | GEO

Human umbilical vein endothelial cells (HUVECs) treated with fenofibrate

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Expression data of human pulmonary arterial smooth muscle cells (PASMCs) treated with BMP-4

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Cytoprotective Effects and Mechanisms of ?-17 Fatty Acid Desaturase in Injured Human Umbilical Vein Endothelial Cells (HUVECs).

Project description:BACKGROUND The beneficial effect of ?-17 FAD is poorly understood. The aim of this study was to investigate the protective mechanism of fatty acids against atherosclerotic (AS) damage induced by oxidized low-density lipoprotein (ox-LDL) in human umbilical vein endothelial cells (HUVECs), and to identify the molecular mechanisms involved. MATERIAL AND METHODS The ox-LDL was used to induce lipotoxicity in HUVECs to establish a model of oxidative injury. HUVECs were transfected with ?-17FAD lentivirus to induce cytoprotective effects. We evaluated the alterations in cell proliferation and apoptosis, and oxidative stress index, including levels of nitric oxide (NO), malonyldialdehyde (MDA), SOD enzyme, LDH, GSH-PX, and vascular endothelial growth factor (VEGF) expression. RESULTS The ox-LDL-induced excessive cellular apoptosis of HUVECs was abrogated by upregulation of ?-17 FAD. Importantly, ?-17 FAD converted ?-3 polyunsaturated fatty acid ARA into ?-6 polyunsaturated fatty acid EPA. Further, ?-17 FAD overexpression promoted the proliferation of HUVECS, and inhibited ox-LDL-induced lipid peroxidation of HUVECs. The levels of nitric oxide, GSH-PX, and SOD enzyme were increased, and the activity of MDA and LDH was suppressed by the upregulation of ?-17 FAD. In addition, upregulation of ?-17 FAD significantly increased VEGF expression. In vitro tube formation assay showed that ?-17 FAD significantly promoted angiogenesis. CONCLUSIONS These results suggest that ?-17 fatty acid desaturase plays a beneficial role in the prevention of ox-LDL-induced cellular damage.

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