Project description:This SuperSeries is composed of the following subset Series: GSE15482: The effect of PPARa siRNA on endothelial cells treated with fenofibrate GSE15483: The effect of fenofibrate on endothelial cells Refer to individual Series
Project description:To determine the role of HBO1 in EC physiology, gene expression analysis was conducted on control and HBO1 siRNA-treated HUVECs. A total of 263 differentially regulated protein-coding transcripts were detected, many of which are key for growth and angiogenesis. Additionally, many genes involved in cell cycle, cell division, and DNA replication were dysregulated. HBO1-regulated genes were verified by qRT-PCR, including those with roles in vessel tone regulation (e.g. ACE1), vessel formation (e.g. CXCL16), EC activation (e.g. E-selectin), and cholesterol efflux (e.g. ABCG1).
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.