title: Genomic-scale analysis of gene expression profiles in TNF-alpha treated human umbilical vein endothelial cells.
abstract: OBJECTIVE
  TNF-alpha is a potent proinflammatory cytokine that plays an important role in immunity and inflammation, and in the control of cell proliferation, differentiation and programmed cell death. However, it is known that TNF-alpha is also the founding member of a still growing family of cytokines with diverse bioregulative functions. Its detailed molecular mechanisms on endothelial activation and injury remain to be elucidated. This study was aimed at determining genomic-scale gene expression profiles in TNF-alpha treated human endothelial cells.
  
  
  METHODS
  In this study cultured human umbilical vein endothelial cells (HUVECs) were stimulated with TNF-alpha (10 ng/ml) for 2 and 16 h, respectively, and the gene expression pattern was profiled using a cDNA array representing 14,000 gene/cDNA clusters.
  
  
  RESULTS
  In total, 72 known human genes were identified the expression levels of which altered over 2-fold in response to TNF-a stimulation. Such alteration was confirmed for IL-8 and MCP-1, with an independent quantitative mRNA assay. It was observed that genes with related biological functions were often temporally co-regulated.
  
  
  CONCLUSIONS
  These results indicate the transcriptional pathways mediated by TNF-alpha inside the HUVECs. Expression profiling in HUVECs responding to TNF-alpha stimulation should give an understanding of the molecular mechanisms involved in vascular inflammation.
authors.affiliation: The National Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing.
authors.forename: J
authors.initials: J
authors.lastname: Zhou
authors.forename: Y
authors.initials: Y
authors.lastname: Jin
authors.forename: Y
authors.initials: Y
authors.lastname: Gao
authors.forename: H
authors.initials: H
authors.lastname: Wang
authors.forename: G
authors.initials: G
authors.lastname: Hu
authors.forename: Y
authors.initials: Y
authors.lastname: Huang
authors.forename: Q
authors.initials: Q
authors.lastname: Chen
authors.forename: M
authors.initials: M
authors.lastname: Feng
authors.forename: C
authors.initials: C
authors.lastname: Wu
mesh_terms: D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000235:genetics; D016000:Cluster Analysis; D018076:DNA, Complementary / Q000096:biosynthesis / Q000235:genetics; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D015870:Gene Expression / Q000187:drug effects*; D015894:Genome, Human; D006801:Humans; D017403:In Situ Hybridization; D016209:Interleukin-8 / Q000096:biosynthesis / Q000235:genetics; D008855:Microscopy, Electron, Scanning; D011247:Pregnancy; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D013056:Spectrophotometry, Ultraviolet; D014158:Transcription, Genetic / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*; D014471:Umbilical Veins / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*
chemical_list: D018932:Chemokine CCL2; D018076:DNA, Complementary; D016209:Interleukin-8; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha