title: [The role of Egr-1 and NF-kappaB in the pathogenesis of silicosis: an in-vitro study].
abstract: OBJECTIVE
  To study the correlation between the expression of Egr-1 and NF-kappaB and the up-regulation of TNF-alpha and TGF-beta1 in macrophages after stimulation by silica in-vitro.
  
  
  METHODS
  Macrophages were treated with antibodies against Egr-1 and NF-kappaB and antisense oligonucleotides. The level of TNF-alpha protein in the cell supernatant was then measured using enzyme-linked immunoadsorbent assay (ELISA). The expression of TGF-beta1 protein was detected by immunocytochemistry. The expression of TNF-alpha and TGF-beta1 mRNAs was also monitored by reverse transcriptase-polymerase chain reaction (RT-PCR).
  
  
  RESULTS
  Compared with silica-stimulated macrophages untreated with antibodies, the cells treated with 10 micro g/ml of Egr-1 or NF-kappaB antibodies were associated with reduced expression of TNF-alpha and TGF-beta1 proteins and mRNAs (P < 0.05). Compared with silica-stimulated untransfected group, the antisense group was associated with obvious reduction in the expression of TNF-alpha and TGF-beta1 proteins and mRNAs (P < 0.05).
  
  
  CONCLUSIONS
  The expression of TNF-alpha and TGF-beta1 mRNAs and proteins are associated with activation of Egr-1 and NF-kappaB in macrophages, after stimulation by silica. It is possible that the corresponding antibodies and antisense oligonucleotides may become a potential therapeutic tool in the management of silicosis in the future.
authors.affiliation: Department of Pathology, Xiangya School of Medicine, Central South University, Changsha 410078, China.
authors.forename: Hai-yan
authors.initials: HY
authors.lastname: Niu
authors.forename: Qing-fu
authors.initials: QF
authors.lastname: Zeng
authors.forename: Xiang
authors.initials: X
authors.lastname: Li
authors.forename: Ling
authors.initials: L
authors.lastname: Chu
authors.forename: Yong-bin
authors.initials: YB
authors.lastname: Hu
authors.forename: Jin-sheng
authors.initials: JS
authors.lastname: Wang
mesh_terms: D000818:Animals; D000906:Antibodies / Q000276:immunology; D002478:Cells, Cultured; D004268:DNA-Binding Proteins / Q000235:genetics / Q000276:immunology*; D051766:Early Growth Response Protein 1; D017874:Immediate-Early Proteins / Q000235:genetics / Q000276:immunology*; D008264:Macrophages / Q000166:cytology / Q000378:metabolism*; D051379:Mice; D016328:NF-kappa B / Q000235:genetics / Q000276:immunology*; D016376:Oligonucleotides, Antisense / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D012822:Silicon Dioxide / Q000494:pharmacology; D012829:Silicosis / Q000209:etiology; D014157:Transcription Factors / Q000235:genetics / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000096:biosynthesis* / Q000235:genetics; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D000906:Antibodies; D004268:DNA-Binding Proteins; D051766:Early Growth Response Protein 1; C486109:Egr1 protein, mouse; D017874:Immediate-Early Proteins; D016328:NF-kappa B; D016376:Oligonucleotides, Antisense; D012333:RNA, Messenger; C508961:Tgfb1 protein, mouse; D014157:Transcription Factors; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; D012822:Silicon Dioxide