Send to:

Choose Destination
See comment in PubMed Commons below
J Formos Med Assoc. 2014 Nov;113(11):828-32. doi: 10.1016/j.jfma.2014.01.008. Epub 2014 Feb 20.

Cyclosporine A induces connective tissue growth factor expression in human gingival fibroblasts: suppression by epigallocatechin-3-gallate.

Author information

  • 1Department of Dentistry, National Taiwan University Hospital Hsinchu Branch, Hsinchu, Taiwan.
  • 2Department of Dentistry, National Taiwan University Hospital, Taipei, Taiwan.
  • 3Department of Dentistry, National Taiwan University Hospital Hsinchu Branch, Hsinchu, Taiwan. Electronic address:



Transforming growth factor-β (TGF-β) plays an important role in the pathogenesis of cyclosporine A (CsA)-induced gingival overgrowth (GO). Connective tissue growth factor (CTGF/CCN2) acts as a cofactor with TGF-β to induce the maximal profibrotic effects of TGF-β. We investigated the effects of CsA on CCN2 expression in human gingival fibroblasts (HGFs) and the potential chemopreventive agent for CsA-induced GO.


Western blot analyses were used to examine the signaling pathways of CsA-induced CCN2 expression in HGFs and whether epigallocatechin-3-gallate (EGCG), curcumin, or lovastatin can inhibit CsA-induced CCN2 expression.


CsA significantly stimulated CCN2 synthesis in HGFs. This effect can be inhibited by c-Jun NH(2)-terminal kinase (JNK) and Smad3 inhibitors but not by TGF-β neutralizing antibody and TGF-β type I receptor inhibitor. Furthermore, EGCG completely blocked CsA-induced CCN2 expression.


CsA-induced CCN2 protein expression is mediated through JNK and Smad signaling. CsA may contribute to the pathogenesis of GO through upregulation of CCN2 expression in HGFs. EGCG could be an adjuvant for the prevention of CsA-induced GO.

Copyright © 2014. Published by Elsevier B.V.


connective tissue growth factor/CCN2; cyclosporine; epigallocatechin-3-gallate; fibroblast; gingival overgrowth

[PubMed - in process]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk