title: [Effects and mechanisms of Egr-1 on inflammatory responses induced by mechanical stress in human periodontal ligament cells].
abstract: OBJECTIVE
  To investigate the effects and mechanisms of silencing Egr-1 on MS-mediated secretion and expression of inflammatory cytokines in hPDLs.
  
  
  METHODS
  The secretion and expression of IL-1β, IL-6, IL-8 and IL-11 were detected using ELISA and RT-PCR when cells were cultured with or without various duration (6, 12, 24 and 48 h) and force (3%, 6%, 12%, 15%) of mechanica stress (MS). RT-PCR and Western blotting were used to evaluate the expression of Egr-1 under a 12% MS for 24 h. The roles of silencing Egr-1 in MS-mediated expression of inflammatory cytokines were determined using ELISA and RT-PCR. The protein levels of PTEN/PI3K/Akt signaling pathway were determined using Western blotting. Moreover, cells were pretreated with 20 μmol/L LY294002 for 30 min, in order to study the mechanisms of Egr-1 in MS-mediated secretion and expression of inflammatory cytokines. Statistical analysis was performed using SPSS 11.0 software package.
  
  
  RESULTS
  The secretion and expression of IL-1β, IL-6, IL-8 and IL-11 were increased gradually with the time under a MS force of 12% in hPDLs, and peaked in cells after exposure to MS for 24 h. The mRNA and protein levels of Egr-1 were elevated in hPDLs after exposure to 12% MS for 24 h. Moreover, depletion of Egr-1 inhibited MS-mediated secretion and expression of inflammatory cytokines. Knockdown of Egr-1 reduced the protein level of PTEN, and increased the protein expression of p-PI3K and p-Akt in hPDLs. LY294002 blocked partially the inhibitory roles of Egr-1 in the secretion and expression of inflammatory cytokines.
  
  
  CONCLUSIONS
  Depletion of Egr-1 suppressed the secretion and expression of inflammatory cytokines induced by MS through PTEN/PI3K/Akt pathway.
authors.affiliation: Department of Prosthodontics, Affiliated Hospital of Yan'an University. Yan'an 716000, Shaanxi Province, China. E-mail:hbo_liu@126.com.
authors.forename: Hai-Yan
authors.initials: HY
authors.lastname: Hu
authors.forename: Zhi-Biao
authors.initials: ZB
authors.lastname: Gao
mesh_terms: D015153:Blotting, Western; D002478:Cells, Cultured; D002867:Chromones; D016207:Cytokines; D051766:Early Growth Response Protein 1 / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D017370:Interleukin-11; D053583:Interleukin-1beta; D015850:Interleukin-6; D016209:Interleukin-8; D009025:Morpholines; D010513:Periodontal Ligament / Q000502:physiology*; D019869:Phosphatidylinositol 3-Kinases; D012333:RNA, Messenger; D015398:Signal Transduction; D013314:Stress, Mechanical
chemical_list: D002867:Chromones; D016207:Cytokines; C497325:EGR1 protein, human; D051766:Early Growth Response Protein 1; C508611:IL11 protein, human; D017370:Interleukin-11; D053583:Interleukin-1beta; D015850:Interleukin-6; D016209:Interleukin-8; D009025:Morpholines; D012333:RNA, Messenger; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; D019869:Phosphatidylinositol 3-Kinases