These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Curcumin inhibits TGFβ1-induced CCN2 via Src, JNK, and Smad3 in gingiva.
    Author: Yang WH, Kuo MY, Liu CM, Deng YT, Chang HH, Chang JZ.
    Journal: J Dent Res; 2013 Jul; 92(7):629-34. PubMed ID: 23609161.
    Abstract:
    Transforming growth factor β (TGFβ) is a key regulator associated with the pathogenesis of gingival overgrowth (GO). Connective tissue growth factor (CTGF/CCN2) is overexpressed in GO tissues. CCN2 promotes and sustains fibrosis initiated by TGFβ. Previous studies have shown that JNK and Smad3 activation is required for TGFβ-induced CCN2 expressions in human gingival fibroblasts (HGFs). In this study, we have found that Src is a major signaling mediator for TGFβ-induced CCN2 expressions in HGFs. Pre-treatment with 2 Src kinase inhibitors (PP2, Src inhibitor-1) significantly reduced TGFβ1-induced CCN2 synthesis and JNK and Smad3 activation in HGFs. These results suggest that Src is an upstream signaling transducer of JNK and Smad3 with respect to TGFβ1-stimulated CCN2 expression in HGFs. We further found that curcumin significantly abrogated the TGFβ1-induced CCN2 in HGFs by inhibiting the phosphorylations of Src, JNK, and Smad3. Furthermore, curcumin inhibited TGFβ1-induced HGF migration and α-SMA expression. Curcumin potentially qualifies as a useful agent for the control of GO.
    [Abstract] [Full Text] [Related] [New Search]