Transforming growth factor-β stimulates Interleukin-11 production by human periodontal ligament and gingival fibroblasts

• Published in: Journal of clinical periodontology 2006-03, Vol.33 (3), p.165-171
• Main Authors: Yashiro, R., Nagasawa, T., Kiji, M., Hormdee, D., Kobayashi, H., Koshy, G., Nitta, H., Ishikawa, I.
• Format: Article
• Language: English
• Subjects: Bone Morphogenetic Protein 2; Bone Morphogenetic Proteins - analysis; Cells, Cultured; Dentistry; Enzyme Activators - pharmacology; Enzyme Inhibitors - pharmacology; Fibroblasts - drug effects; Fibroblasts - immunology; Flow Cytometry; Gingiva - cytology; Gingiva - drug effects; Gingiva - immunology; Humans; interleukin-11; Interleukin-11 - analysis; Interleukin-11 - biosynthesis; periodontal fibroblasts; Periodontal Ligament - cytology; Periodontal Ligament - drug effects; Periodontal Ligament - immunology; protein kinase C; Protein Kinase C - antagonists & inhibitors; Receptors, Transforming Growth Factor beta - analysis; RNA, Messenger - analysis; Transforming Growth Factor beta - analysis; Transforming Growth Factor beta - pharmacology; Up-Regulation
• ISSN: 0303-6979; 1600-051X
• DOI: 10.1111/j.1600-051X.2006.00898.x

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.