title: A key mediator, PTX3, of IKK/IκB/NF-κB exacerbates human umbilical vein endothelial cell injury and dysfunction.
abstract: OBJECTIVE
  This study was performed to investigate PTX3-mediated iNOS expression and IKK/IκB/NF-κB activation in PA-induced atherosclerotic HUVECs injury model.
  
  
  METHODS
  The cell viability was detected by the CCK8 assay. The cell apoptosis was assessed by annexin V-PI double-labeling staining. Expression of genes and proteins were analyzed by real-time PCR and western blotting respectively. Cells were transfected with siRNAs as a gene silencing methods.
  
  
  RESULTS
  PA induced cell apoptosis in human umbilical vein endothelial cells in a time and dose-dependent manner. PA also induced upregulation expression of PTX3. TPCA-1, an inhibitor of IKK-2, could suppress the expression of PTX3 and phospho-IκB-α in PA-induced endothelial dysfunction cell model. We also found that transfection of cells with PTX3 siRNA reduced the expression of iNOS and NO, and protected PA-induced cell apoptosis in HUVECs.
  
  
  CONCLUSIONS
  PTX3 could exacerbate endothelial dysfunction, at least partially, through IKK/IκB/NF-κB activation and overexpression of iNOS and NO, and advance the development of atherosclerosis.
authors.affiliation: Department of Cardiovascular Surgery, Fourth Hospital of Hebei Medical University Shijiazhuang, China.
authors.forename: Yongbo
authors.initials: Y
authors.lastname: Zhao
authors.affiliation: Department of Cardiovascular Surgery, Fourth Hospital of Hebei Medical University Shijiazhuang, China.
authors.forename: Guangxing
authors.initials: G
authors.lastname: Feng
authors.affiliation: Department of Cardiovascular Surgery, Fourth Hospital of Hebei Medical University Shijiazhuang, China.
authors.forename: Yanzhi
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Neurology, Hebei General Hospital Shijiazhuang, China.
authors.forename: Yuehong
authors.initials: Y
authors.lastname: Yue
authors.affiliation: Department of Cardiovascular Surgery, Fourth Hospital of Hebei Medical University Shijiazhuang, China.
authors.forename: Weichao
authors.initials: W
authors.lastname: Zhao
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D050197:Atherosclerosis / Q000378:metabolism / Q000473:pathology; D002097:C-Reactive Protein / Q000235:genetics / Q000378:metabolism*; D002470:Cell Survival / Q000187:drug effects; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D020672:I-kappa B Proteins / Q000378:metabolism*; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D019308:Palmitic Acid / Q000494:pharmacology; D000683:Serum Amyloid P-Component / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D000099153:Pentraxins
chemical_list: D002097:C-Reactive Protein; D020672:I-kappa B Proteins; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D019308:Palmitic Acid; D000683:Serum Amyloid P-Component; D000099153:Pentraxins; C000606204:NFKBIA protein, human
keywords: HUVECs; NF-κB; PTX3; atherosclerosis; iNOS