Tags

Type your tag names separated by a space and hit enter

Catechins inhibit CXCL10 production from oncostatin M-stimulated human gingival fibroblasts.

Abstract

CXC chemokine ligand 10 (CXCL10) plays a pivotal role in the recruitment of Th1 cells and, thus, in the development of periodontal disease. Epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), the major catechins derived from green tea, have multiple beneficial effects, but the effects of catechins on CXCL10 production from human gingival fibroblasts (HGFs) is not known. In this study, we investigated the mechanisms by which EGCG and ECG inhibit oncostatin M (OSM)-induced CXCL10 production in HGFs. HGFs constitutively expressed glycoprotein 130 and OSM receptor beta (OSMR beta), which are OSM receptors. OSM increased CXCL10 production in a concentration-dependent manner. EGCG and ECG prevented OSM-mediated CXCL10 production by HGFs. Inhibitors of p38 mitogen-activated protein kinase, c-Jun N-terminal kinase (JNK), phosphatidylinositol-3-OH kinase and signal transducer and activator of transcription (STAT)3 decreased OSM-induced CXCL10 production. EGCG significantly prevented OSM-induced phosphorylation of JNK, Akt (Ser473) and STAT3 (Tyr705 and Ser727). ECG prevented phosphorylation of JNK and Akt (Ser473). In addition, EGCG and ECG attenuated OSMR beta expression on HGFs. These data provide a novel mechanism through which the green tea flavonoids, catechins, can provide direct benefits in periodontal disease.

Links

  • Publisher Full Text
  • Authors+Show Affiliations

    ,

    Department of Conservative Dentistry and Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Tokushima 770-8504, Japan. hosokawa@dent.tokushima-u.ac.jp

    , , , ,

    Source

    MeSH

    Anti-Inflammatory Agents, Non-Steroidal
    Antioxidants
    Catechin
    Cells, Cultured
    Chemokine CXCL10
    Cytokine Receptor gp130
    Enzyme Inhibitors
    Fibroblasts
    Gene Expression Regulation
    Gingiva
    Humans
    Oncostatin M
    Oncostatin M Receptor beta Subunit
    Osmolar Concentration
    Periodontal Diseases
    Phosphorylation
    Signal Transduction

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    19616927

    Citation

    Hosokawa, Yoshitaka, et al. "Catechins Inhibit CXCL10 Production From Oncostatin M-stimulated Human Gingival Fibroblasts." The Journal of Nutritional Biochemistry, vol. 21, no. 7, 2010, pp. 659-64.
    Hosokawa Y, Hosokawa I, Ozaki K, et al. Catechins inhibit CXCL10 production from oncostatin M-stimulated human gingival fibroblasts. J Nutr Biochem. 2010;21(7):659-64.
    Hosokawa, Y., Hosokawa, I., Ozaki, K., Nakanishi, T., Nakae, H., & Matsuo, T. (2010). Catechins inhibit CXCL10 production from oncostatin M-stimulated human gingival fibroblasts. The Journal of Nutritional Biochemistry, 21(7), pp. 659-64. doi:10.1016/j.jnutbio.2009.04.005.
    Hosokawa Y, et al. Catechins Inhibit CXCL10 Production From Oncostatin M-stimulated Human Gingival Fibroblasts. J Nutr Biochem. 2010;21(7):659-64. PubMed PMID: 19616927.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Catechins inhibit CXCL10 production from oncostatin M-stimulated human gingival fibroblasts. AU - Hosokawa,Yoshitaka, AU - Hosokawa,Ikuko, AU - Ozaki,Kazumi, AU - Nakanishi,Tadashi, AU - Nakae,Hideaki, AU - Matsuo,Takashi, Y1 - 2009/07/18/ PY - 2008/11/21/received PY - 2009/04/06/revised PY - 2009/04/13/accepted PY - 2009/7/21/entrez PY - 2009/7/21/pubmed PY - 2010/10/6/medline SP - 659 EP - 64 JF - The Journal of nutritional biochemistry JO - J. Nutr. Biochem. VL - 21 IS - 7 N2 - CXC chemokine ligand 10 (CXCL10) plays a pivotal role in the recruitment of Th1 cells and, thus, in the development of periodontal disease. Epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), the major catechins derived from green tea, have multiple beneficial effects, but the effects of catechins on CXCL10 production from human gingival fibroblasts (HGFs) is not known. In this study, we investigated the mechanisms by which EGCG and ECG inhibit oncostatin M (OSM)-induced CXCL10 production in HGFs. HGFs constitutively expressed glycoprotein 130 and OSM receptor beta (OSMR beta), which are OSM receptors. OSM increased CXCL10 production in a concentration-dependent manner. EGCG and ECG prevented OSM-mediated CXCL10 production by HGFs. Inhibitors of p38 mitogen-activated protein kinase, c-Jun N-terminal kinase (JNK), phosphatidylinositol-3-OH kinase and signal transducer and activator of transcription (STAT)3 decreased OSM-induced CXCL10 production. EGCG significantly prevented OSM-induced phosphorylation of JNK, Akt (Ser473) and STAT3 (Tyr705 and Ser727). ECG prevented phosphorylation of JNK and Akt (Ser473). In addition, EGCG and ECG attenuated OSMR beta expression on HGFs. These data provide a novel mechanism through which the green tea flavonoids, catechins, can provide direct benefits in periodontal disease. SN - 1873-4847 UR - https://www.unboundmedicine.com/medline/citation/19616927/Catechins_inhibit_CXCL10_production_from_oncostatin_M_stimulated_human_gingival_fibroblasts_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0955-2863(09)00089-8 DB - PRIME DP - Unbound Medicine ER -