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Transforming growth factor‐ β stimulates Interleukin‐11 production by human periodontal ligament and gingival fibroblasts
Author(s) -
Yashiro R.,
Nagasawa T.,
Kiji M.,
Hormdee D.,
Kobayashi H.,
Koshy G.,
Nitta H.,
Ishikawa I.
Publication year - 2006
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/j.1600-051x.2006.00898.x
Subject(s) - periodontal fiber , transforming growth factor , cytokine , chemistry , activator (genetics) , interleukin , transforming growth factor beta , bone morphogenetic protein 2 , receptor , microbiology and biotechnology , medicine , endocrinology , biology , in vitro , dentistry , biochemistry
Background: Transforming growth factor (TGF)‐ β is a potent multifunctional polypeptide, abundant in the bone matrix. Interleukin (IL)‐11 is a pleiotropic cytokine with effects on multiple cell types. The present study was performed to evaluate the regulatory effects of TGF‐ β on IL‐11 production by human periodontal ligament cells (PDL) and human gingival fibroblasts (HGF). Material and Methods: The expression of TGF‐ β receptor in PDL and HGF were observed using flow cytometry. PDL and HGF were stimulated with TGF‐ β with or without protein kinase C (PKC) inhibitors and activator. IL‐11, bone morphogenetic protein‐2 (BMP‐2) and TGF‐ β mRNA expression was quantified by real‐time polymerase chain reaction (PCR). IL‐11 production was measured using enzyme‐linked immunosorbent assay. Results: PDL and HGF expressed both TGF‐ β receptor I and TGF‐ β receptor II on the cell surfaces. IL‐11 mRNA expression and IL‐11 production were augmented by TGF‐ β in both PDL and HGF, with higher values in PDL. PKC inhibitors partially suppressed TGF‐ β ‐induced IL‐11 production in PDL and HGF, whereas activator enhanced it. TGF‐ β mRNA and BMP‐2 mRNA expression were up‐regulated by TGF‐ β in PDL. Conclusion: These results suggest that PDL produce IL‐11 in response to TGF‐ β .