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Impairment of Gingival Fibroblast Adherence by IL-6/sIL-6RDepartment of Patho-physiology Periodontal Science, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8525, Japan
Department of Patho-physiology Periodontal Science, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8525, Japan
Department of Patho-physiology Periodontal Science, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8525, Japan
Taipei Medical College School of Dentistry, Taipei, Taiwan, ROC
Department of Patho-physiology Periodontal Science, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8525, Japan
Department of Patho-physiology Periodontal Science, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8525, Japan
Department of Patho-physiology Periodontal Science, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8525, Japan
Interleukin-6 (IL-6) binds to human gingival fibroblasts (HGF) in the presence of a soluble form of IL-6 receptor (sIL-6R). We investigated the effects of IL-6 on the functions of HGF in the presence of sIL-6R. HGF changed their morphology from spindle-shaped to round, and detached from the culture dish by stimulation with IL-6/sIL-6R. In this condition, a signal transducer gpl30 and a transcription factor Stat3 were phosphorylated, resulting in activation of transcription factors Stat3 and C/EBPβ. Cytoskeletal β-actin and adhesion molecule integrin-a5, a subunit of
Key Words: gingival fibroblast adherence IL-6/sIL-6R actin VLA-5.
Journal of Dental Research, Vol. 80, No. 5,
1421-1424 (2001) This article has been cited by other articles:
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5β1 integrin (VLA-5), were found to possess potential binding domains for these transcription factors in their promoters. Accumulation of (3-actin and integrin-a5 mRNA decreased, contrary to the expectation of the induction of gene transcription. Furthermore, the decrease in their mRNAs was associated with reduced expression of both actin and VLA-5 proteins. These results suggest that the expression of VLA-5 and actin was down-regulated in HGF through an IL-6 signaling pathway, resulting in impairment of HGF adherence. 