Inhibition of elastin and collagen networks degradation in human skin by gingival fibroblast. In vitro, ex vivo and in vivo studies.

HTML  Download Download as PDF (Size: 992KB)  PP. 4-14  
DOI: 10.4236/jcdsa.2011.11002    5,921 Downloads   12,596 Views  Citations

Affiliation(s)

.

ABSTRACT

Skin aging shows an imbalance between synthesis and degradation of the extracellular matrix. The overproduction of degradative enzymes (MMPs) during the chronology- and photo-induced aging leads to a degradation of the elastic and collagen networks. In a model of collagen and elastin destruction, we showed that the gingival fibroblast was able to preserve these macromolecules by inhibiting the overproduction of metalloproteinases by overproduction of TIMP-1 and modulation of the inflammatory cytokines activity. The objective of this study is to evaluate the effect of the gingival fibroblasts on human skin. The results in vitro and ex vivo show that the gingival fibroblast protects the skin collagen and elastic network by the inhibition of MMPs which leads to an overproduction of the TIMP-1. Moreover, the gingival fibroblast modulates the activity of some enzymes responsible for the inflammation; they inhibit the IL-1β and stimulate the production of TGF-β1. In vivo studies with a duration of six months and 50 women with pronounced wrinkles show that the culture supernatant of gingival fibroblasts diluted to 5% leads to a statistically significant decrease in the number and length of wrinkles.

Share and Cite:

B. Gogly, F. Ferré, H. Cherifi, A. Naveau and B. Fournier, "Inhibition of elastin and collagen networks degradation in human skin by gingival fibroblast. In vitro, ex vivo and in vivo studies.," Journal of Cosmetics, Dermatological Sciences and Applications, Vol. 1 No. 1, 2011, pp. 4-14. doi: 10.4236/jcdsa.2011.11002.

Copyright © 2024 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.