title: Expression of suppressor of cytokine signaling 1 and 3 in ligature-induced periodontitis in rats.
abstract: OBJECTIVE
  Evaluate expression of inducible negative regulators of JAK/STAT pathway and their target proteins during the course of ligature-induced experimental periodontal disease in rats.
  
  
  METHODS
  Rats were sacrificed 07, 15 and 30 days after disease induction for histological evaluation of periodontal inflammation and macroscopic analysis of alveolar bone loss. SOCS expression and the activation status of STAT1 and STAT3 were evaluated in gingival biopsies by real time PCR and Western blot.
  
  
  RESULTS
  Ligature-induced model presented significant progressive bone loss from 7 to 30 days. Inflammation was evident and similar for 07 and 15 days; however, a decrease on severity at the end of the experimental period was observed. There was a significant (p<0.05) increase on SOCS1 and SOCS3 gene expression in PD compared to control group at 15 and 30days. The SOCS1 and SOCS3 protein expression and activation of STAT1 and STAT3 were increased in earlier periods in the ligature model.
  
  
  CONCLUSIONS
  This study suggests that SOCS1 and SOCS3 were directly correlated with regulatory mechanism of the inflammatory process responsible for the periodontal disease destruction.
authors.affiliation: Department of Diagnosis and Surgery, School of Dentistry at Araraquara, Univ Estadual Paulista - UNESP, Rua Humaita, 1680-Centro, Araraquara, SP, 14801-903, Brazil.
authors.forename: João Antonio Chaves
authors.initials: JA
authors.lastname: de Souza
authors.forename: Andressa Vilas Boas
authors.initials: AV
authors.lastname: Nogueira
authors.forename: Pedro Paulo Chaves
authors.initials: PP
authors.lastname: de Souza
authors.forename: Joni Augusto
authors.initials: JA
authors.lastname: Cirelli
authors.forename: Gustavo Pompermaier
authors.initials: GP
authors.lastname: Garlet
authors.forename: Carlos
authors.initials: C
authors.lastname: Rossa
mesh_terms: D016301:Alveolar Bone Loss / Q000378:metabolism / Q000473:pathology; D000818:Animals; D003094:Collagen / Q000032:analysis; D003238:Connective Tissue / Q000473:pathology; D004195:Disease Models, Animal; D005347:Fibroblasts / Q000473:pathology; D005881:Gingiva / Q000378:metabolism / Q000473:pathology; D007091:Image Processing, Computer-Assisted / Q000379:methods; D016753:Interleukin-10 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D053612:Janus Kinases / Q000032:analysis; D008297:Male; D053244:Osteoprotegerin / Q000032:analysis; D010518:Periodontitis / Q000378:metabolism* / Q000473:pathology; D053245:RANK Ligand / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D050791:STAT Transcription Factors / Q000032:analysis; D050794:STAT1 Transcription Factor; D050796:STAT3 Transcription Factor; D015398:Signal Transduction / Q000502:physiology*; D000071222:Suppressor of Cytokine Signaling 1 Protein; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000032:analysis*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D015850:Interleukin-6; D053244:Osteoprotegerin; D053245:RANK Ligand; D050791:STAT Transcription Factors; D050794:STAT1 Transcription Factor; D050796:STAT3 Transcription Factor; C491589:Socs1 protein, rat; C491410:Socs3 protein, rat; C494081:Stat1 protein, rat; C494088:Stat3 protein, rat; D000071222:Suppressor of Cytokine Signaling 1 Protein; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins; C506032:Tnfrsf11b protein, rat; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D003094:Collagen; D053612:Janus Kinases