title: Expression levels of adiponectin receptors and periodontitis.
abstract: OBJECTIVE
  We recently showed that adiponectin, an adipocyte-derived cytokine, may function as a negative regulator of the Toll-like receptor signaling pathway and of osteoclast formation in periodontal disease. In this study, we investigated whether the expression levels of adiponectin receptors (AdipoR1 and AdipoR2) are related to the presence of periodontitis.
  
  
  METHODS
  We initially examined, using RT-PCR, the expression of the AdipoR1 and AdipoR2 genes at the mRNA level in several oral tissues of C57BL mice. Next, we investigated (using real-time PCR assays) whether inflammatory cytokines, such as tumor necrosis factor-alpha, could affect the expression levels of these genes in human gingival fibroblasts. Lastly, we compared the expression levels of these receptor proteins in gingival tissues between two healthy subjects and five patients with severe periodontal disease using western blotting analysis.
  
  
  RESULTS
  The AdipoR1 and AdipoR2 receptors were ubiquitously expressed in the oral tissues of mice. We observed that treatment with tumor necrosis factor-alpha could significantly reduce the expression levels of both AdipoR1 and AdipoR2 genes in human gingival fibroblasts. Moreover, we found that the expression of both receptors was lower in periodontal tissues from patients with severe periodontitis than in patients with healthy periodontal tissues.
  
  
  CONCLUSIONS
  These observations suggest that adiponectin may not function efficiently in sites of periodontal disease because of a decrease in the number of its receptors, and this probable dysfunction may play a role in worsening periodontitis in patients.
authors.affiliation: Section of Pediatric Dentistry, Division of Oral Health, Growth and Development, Faculty of Dental Science, Kyushu University, Fukuoka, Japan. nyama@dent.kyushu-u.ac.jp
authors.forename: N
authors.initials: N
authors.lastname: Yamaguchi
authors.forename: T
authors.initials: T
authors.lastname: Hamachi
authors.forename: N
authors.initials: N
authors.lastname: Kamio
authors.forename: S
authors.initials: S
authors.lastname: Akifusa
authors.forename: K
authors.initials: K
authors.lastname: Masuda
authors.forename: Y
authors.initials: Y
authors.lastname: Nakamura
authors.forename: K
authors.initials: K
authors.lastname: Nonaka
authors.forename: K
authors.initials: K
authors.lastname: Maeda
authors.forename: S
authors.initials: S
authors.lastname: Hanazawa
authors.forename: Y
authors.initials: Y
authors.lastname: Yamashita
mesh_terms: D000368:Aged; D000818:Animals; D002460:Cell Line; D002478:Cells, Cultured; D055113:Chronic Periodontitis / Q000378:metabolism; D016207:Cytokines / Q000494:pharmacology; D005260:Female; D005347:Fibroblasts / Q000378:metabolism; D005881:Gingiva / Q000378:metabolism; D005891:Gingivitis / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008875:Middle Aged; D010514:Periodontal Pocket / Q000378:metabolism; D010518:Periodontitis / Q000378:metabolism*; D054419:Receptors, Adiponectin / Q000032:analysis* / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: C475418:ADIPOR1 protein, human; C475420:ADIPOR2 protein, human; D016207:Cytokines; D018836:Inflammation Mediators; D054419:Receptors, Adiponectin; D014409:Tumor Necrosis Factor-alpha; C475419:adiponectin receptor 1, mouse; C475421:adiponectin receptor 2, mouse