Format

Send to

Choose Destination
See comment in PubMed Commons below
J Dermatol Sci. 2010 Feb;57(2):108-13. doi: 10.1016/j.jdermsci.2009.11.007. Epub 2010 Jan 8.

Glycolic acid induces keratinocyte proliferation in a skin equivalent model via TRPV1 activation.

Author information

  • 1Shiseido Research Center, 2-12-1 Fukuura, Kanazawa-ku, Yokohama 236-8643, Japan.

Abstract

BACKGROUND:

Glycolic acid (GA) is the most commonly used alpha-hydroxy acid (AHA) for dermatologic applications, and is considered as a versatile superficial peeling agent for facial rejuvenation. Its therapeutic effect includes acceleration of epidermal turnover without apparent inflammation, and its action is pH-dependent. However, little is known about the molecular mechanism of GA-induced peeling.

OBJECTIVE:

To investigate the effects of topical application of GA on cell proliferation using a skin equivalent model and to examine the molecular mechanisms of GA-induced peeling.

METHODS:

GA solution was applied on the surface of a skin equivalent model, and cell proliferation was measured by means of BrdU-incorporation and immunohistochemical methods. Release of chemical mediators such as ATP into the medium was examined. The effects of antagonists of ion channels were also analyzed.

RESULTS:

At 24h after GA application, BrdU-incorporation into basal keratinocytes was significantly increased. Induction of keratinocyte proliferation was pH-dependent, and was inhibited by antagonists of TRPV1, an acid-sensitive ion channel. Furthermore, transient ATP release was detected in the culture medium after GA stimulation, and this was also suppressed by TRPV1 antagonists.

CONCLUSION:

These results suggest that one of the mechanisms of GA-induced epidermal proliferation is a growth response of basal keratinocytes to the local elevation of H(+)-ion concentration by infiltrated GA. This response is mediated by TRPV1 activation and ATP release. Activation of P2 receptors by the released ATP may also be involved.

PMID:
20060270
DOI:
10.1016/j.jdermsci.2009.11.007
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center