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

ABSTRACT: 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.

SUBMITTER: Zhou H

PROVIDER: S-EPMC5388310 | biostudies-literature | 2017 Apr

REPOSITORIES: biostudies-literature

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

Zhou Haoyu H Wang Chengming C

Medical science monitor : international medical journal of experimental and clinical research 20170404

BACKGROUND The beneficial effect of Δ-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 Δ-17FAD lentivi ...[more]

PMID: 28373637

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Project description:BackgroundErectile dysfunction (ED) is a well-known complication of diabetes, affecting up to 75% of diabetic men. Although the etiology of diabetic ED is multifactorial, endothelial dysfunction is considered to be a pillar of its pathophysiology. Endothelial dysfunction is caused by the harmful effects of high glucose levels and increased oxidative stress on the endothelial cells that comprise the vascular endothelium. The aim of this study was to identify the proteomic changes caused by high glucose-induced oxidative stress and explore the role of heme oxygenase 1 (HMOX1) in it.MethodsThe cellular proteomic response to hypoxanthine-induced oxidative stress in human umbilical vein endothelial cells (HUVECs) was analyzed by isobaric tags for relative and absolute quantitation (iTRAQ) combined with liquid chromatography-tandem mass spectrometry (LC-MS/MS). Differentially expressed proteins (DEPs) were analyzed through Network and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Further validation assays was performed to validate the role of HMOX1.ResultsThe results showed that 66 and 76 DEPs were markedly upregulated and downregulated, respectively, for HUVECs oxidative stress. Among these proteins, we verified eight dysregulated genes by quantitative reverse transcription PCR, including nucleolin (NCL), X-ray repair cross-complementing protein 6 (XRCC6), ubiquinol-cytochrome C reductase binding protein (UQCRB), non-POU domain containing octamer binding (NONO), heme oxygenase 1 (HMOX1), nucleobindin 1 (NUCB1), DEK, and chromatin target of prmt1 (CHTOP). Further, using overexpression and genetic knockdown approaches, we found that HMOX1 was critical for the oxidative stress response in HUVECs.ConclusionsWe found that HMOX1 was closely related to the oxidative stress response induced by hypoxanthine. To the best of our knowledge, this study is the first overview of the responses of HUVECs to oxidative stress. The findings will contribute to analyses of the detailed molecular mechanisms involved in the pathogenesis of endothelial dysfunction and related molecular mechanisms in ED patients.

Dataset Information

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

Publications

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

Similar Datasets

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