title: Regulation of matrix metalloproteinases, tissue inhibitor of matrix metalloproteinase-1, and extracellular metalloproteinase inducer by interleukin-17 in human periodontal ligament fibroblasts.
abstract: BACKGROUND
  Under physiological conditions, matrix metalloproteinases (MMPs) are involved in the turnover of periapical tissue, and their activity is tightly regulated by tissue inhibitors of metalloproteinases (TIMPs). Disturbances in the balance between MMPs and TIMPs may result in excessive tissue destruction. In addition, the extracellular metalloproteinase inducer (EMMPRIN) capable of inducing MMPs may also play a role in the pathologic processes. This study aimed to investigate the effects of interleukin (IL)-17 on the mRNA expression and protein production of MMP-1, MMP-2, MMP-9, MMP-13, TIMP-1, and EMMPRIN through human periodontal ligament cells.
  
  
  METHODS
  The cells were stimulated with IL-17 (1, 10, and 50 ng/mL) for different time periods. The mRNA levels of MMP-1, MMP-2, MMP-9, MMP-13, TIMP-1, and EMMPRIN were evaluated via quantitative real-time polymerase chain reaction analysis, whereas the protein secretion into the culture medium was assessed via enzyme-linked immunosorbent assay and zymography analysis.
  
  
  RESULTS
  IL-17 significantly up-regulated MMP-1 and MMP-13 mRNA expression but down-regulated MMP-2, MMP-9, and TIMP-1 mRNA expression. Furthermore, IL-17 (50 ng/mL) increased the secreted protein level of MMP-1 and MMP-13 and conversely reduced the level of MMP-2, MMP-9, and TIMP-1. However, IL-17 exerted no effect on EMMPRIN mRNA or protein secretion.
  
  
  CONCLUSIONS
  This study first reported the ability of IL-17 to regulate MMP and TIMP-1 production through human periodontal ligament cells, a phenomenon that may contribute to periapical tissue destruction.
authors.affiliation: State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Wu
authors.forename: Lingxin
authors.initials: L
authors.lastname: Zhu
authors.forename: Hongxia
authors.initials: H
authors.lastname: Wei
authors.forename: Bin
authors.initials: B
authors.lastname: Peng
mesh_terms: D051926:Basigin / Q000187:drug effects*; D018929:Cell Culture Techniques; D004305:Dose-Response Relationship, Drug; D004797:Enzyme-Linked Immunosorbent Assay; D005347:Fibroblasts / Q000201:enzymology*; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D006801:Humans; D018836:Inflammation Mediators / Q000494:pharmacology; D020381:Interleukin-17 / Q000494:pharmacology*; D020781:Matrix Metalloproteinase 1 / Q000187:drug effects; D053509:Matrix Metalloproteinase 13 / Q000187:drug effects; D020778:Matrix Metalloproteinase 2 / Q000187:drug effects; D020780:Matrix Metalloproteinase 9 / Q000187:drug effects; D020782:Matrix Metalloproteinases / Q000187:drug effects*; D010486:Periapical Tissue / Q000166:cytology / Q000201:enzymology; D010513:Periodontal Ligament / Q000166:cytology / Q000201:enzymology*; D011480:Protease Inhibitors / Q000032:analysis*; D012333:RNA, Messenger / Q000187:drug effects; D060888:Real-Time Polymerase Chain Reaction; D013997:Time Factors; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000187:drug effects*
chemical_list: C497886:BSG protein, human; D018836:Inflammation Mediators; D020381:Interleukin-17; D011480:Protease Inhibitors; D012333:RNA, Messenger; C560822:TIMP1 protein, human; D019715:Tissue Inhibitor of Metalloproteinase-1; D051926:Basigin; C507079:MMP13 protein, human; D053509:Matrix Metalloproteinase 13; D020782:Matrix Metalloproteinases; C522361:MMP2 protein, human; D020778:Matrix Metalloproteinase 2; C579270:MMP9 protein, human; D020780:Matrix Metalloproteinase 9; C522360:MMP1 protein, human; D020781:Matrix Metalloproteinase 1