title: Cyclophilin A (CypA) is associated with the inflammatory infiltration and alveolar bone destruction in an experimental periodontitis.
abstract: OBJECTIVE
  CypA is able to regulate inflammatory responses and MMPs production via interaction with its cell surface receptor, EMMPRIN. This study aimed to address the possible association of CypA with pathological inflammation and destruction of periodontal tissues, and whether CypA-EMMPRIN interaction exists in periodontitis.
  
  
  METHODS
  Experimental periodontitis was induced by ligation according to our previous method. Histological and radiographic examinations were performed. Western blot was used to detect CypA and EMMPRIN expressions in gingival tissues. Immunohistochemistry was applied for CypA, EMMPRIN, MMP-1, MMP-2, MMP-9, as well as cell markers of macrophage, lymphocyte and neutrophil. CypA expression, alveolar bone loss, and inflammatory infiltrations were quantified followed by correlation analyses.
  
  
  RESULTS
  Western blot revealed that CypA and EMMRPIN expressions were dramatically elevated in inflamed gingival tissues (ligature group) as compared to healthy gingival tissues (control group). The enhanced CypA and EMMPRIN expressions were highly consistent in cell localization on seriate sections. They were permanently co-localized in infiltrating macrophages and lymphocytes, as well as osteoclasts and osteoblasts in interradicular bone, but rarely expressed by infiltrating neutrophils. MMP-1, MMP-2, and MMP-9 expressions were also sharply increased in inflamed gingiva. MMP-2 and MMP-9 were mainly over-expressed by macrophages, while MMP-1 was over-produced by fibroblasts and infiltrating cells. The number of CypA-positive cells was strongly correlated with the ACJ-AC distance (r=0.839, p=0.000), the number of macrophages (r=0.972, p=0.000), and the number of lymphocytes (r=0.951, p=0.000).
  
  
  CONCLUSIONS
  CypA is associated with the inflammatory infiltration and alveolar bone destruction of periodontitis. CypA-EMMPRIN interaction may exist in these pathological processes.
authors.affiliation: Key Laboratory for Oral Biomedical Engineering of Ministry of Education, School & Hospital of Stomatology, Wuhan University, 237 Luo Yu Road, Hongshan District, Wuhan 430079, China.
authors.forename: Lihua
authors.initials: L
authors.lastname: Liu
authors.forename: Chengzhang
authors.initials: C
authors.lastname: Li
authors.forename: Cia
authors.initials: C
authors.lastname: Cai
authors.forename: Junbo
authors.initials: J
authors.lastname: Xiang
authors.forename: Zhengguo
authors.initials: Z
authors.lastname: Cao
mesh_terms: D016301:Alveolar Bone Loss / Q000000981:diagnostic imaging / Q000201:enzymology* / Q000473:pathology; D000818:Animals; D051926:Basigin / Q000378:metabolism*; D021984:Cyclophilin A / Q000378:metabolism*; D004195:Disease Models, Animal; D008297:Male; D020781:Matrix Metalloproteinase 1 / Q000378:metabolism; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D010518:Periodontitis / Q000000981:diagnostic imaging / Q000201:enzymology* / Q000473:pathology; D011859:Radiography; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D051926:Basigin; D020778:Matrix Metalloproteinase 2; C522363:Mmp2 protein, rat; D020780:Matrix Metalloproteinase 9; D020781:Matrix Metalloproteinase 1; D021984:Cyclophilin A