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Cytokines differentially regulate ICAM‐1 and VCAM‐1 expression on human gingival fibroblasts
Author(s) -
Hosokawa Y.,
Hosokawa I.,
Ozaki K.,
Nakae H.,
Matsuo T.
Publication year - 2006
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.2006.03064.x
Subject(s) - vcam 1 , icam 1 , tumor necrosis factor alpha , intercellular adhesion molecule 1 , mapk/erk pathway , biology , kinase , proinflammatory cytokine , cell adhesion molecule , transforming growth factor , microbiology and biotechnology , chemistry , immunology , cancer research , inflammation
The expression of intercellular adhesion molecule‐1 (ICAM‐1) and vascular adhesion molecule‐1 (VCAM‐1) on human gingival fibroblasts (HGF) may be important for migration and retention of inflammatory cells in periodontally diseased tissue. This study aimed to assess which cytokines regulate ICAM‐1 and VCAM‐1 expression on HGF. Tumour necrosis factor (TNF)‐α and interferon (IFN)‐γ enhanced both ICAM‐1 and VCAM‐1 expression on HGF. Interleukin (IL)‐1β mainly up‐regulated ICAM‐1 expression. On the other hand, IL‐4 and IL‐13 enhanced only VCAM‐1 expression on HGF. IL‐10 did not modulate both ICAM‐1 and VCAM‐1 expression. Transforming growth factor (TGF)‐β1 enhanced ICAM‐1 expression. However, TGF‐β1 inhibited the VCAM‐1 expression induced by TNF‐α or IL‐4. Both ICAM‐1 and VCAM‐1 expression by HGF was inhibited by nuclear factor‐kappaB (NF‐κB) activation inhibitor (MG‐132). Mitogen‐activated protein kinases (MAPK) inhibitors did not influence ICAM‐1 expression induced by TNF‐α. Interestingly, VCAM‐1 expression was enhanced by MEK inhibitor (PD98059) and c‐Jun NH2‐terminal kinase (JNK) inhibitor (SP600125). These results mean that the balance of cytokines in periodontally diseased tissue may be essential for control of ICAM‐1 and VCAM‐1 expression on HGF, and the balance of ICAM‐1 and VCAM‐1 expression might be important for regulation of leucocytes infiltration and retention in periodontally diseased tissue.

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