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Accelerated Wound Healing by S-Methylmethionine Sulfonium: Evidence of Dermal Fibroblast Activation via the ERK1/2 Pathway

Authors
Kim, Won-SerkYang, You JinMin, Hyung GeunSong, Min GyuLee, Ji-SeonPark, Keung-YoungKim, Jin-JuSung, Jong-HyukChoi, Jun-SeokCha, Hyuk-Jin
Issue Date
2010
Publisher
KARGER
Keywords
S-methylmethionine sulfonium; Wound healing; Proliferation; Migration; ERK1/2 pathway
Citation
PHARMACOLOGY, v.85, no.2, pp.68 - 76
Indexed
SCIE
SCOPUS
Journal Title
PHARMACOLOGY
Volume
85
Number
2
Start Page
68
End Page
76
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/118697
DOI
10.1159/000276495
ISSN
0031-7012
Abstract
S-Methylmethionine sulfonium (SMMS) is a derivative of the amino acid methionine, and is synthesized in a variety of plants. SMMS is widely referred to as vitamin U because of its potent therapeutic effect on gastrointestinal ulceration. Skin wounds are accompanied by mucosal erosion and share similar histopathological aspects with gastric ulcers, so it is plausible that SMMS may promote skin wound healing. In animal models, topical administration of SMMS for a given period of time, to both physical and chemical wounds, facilitated wound closure and promoted re-epithelialization compared with a control. In addition, single SMMS treatment was sufficient to promote the growth of human dermal fibroblasts (hDFs) as well as the migration of hDFs, which are indispensable steps for skin wound healing. The promotion of hDF proliferation and migration resulted from considerable activation of ERK1/2 by SMMS, and inhibition of ERK activity by a chemical inhibitor significantly abrogated both the promoted proliferation and migration of hDFs. Therefore, we concluded that SMMS facilitated the repair process of skin damage by activation of dermal fibroblasts, which suggests that SMMS has potential as a skin wound-healing agent. Copyright (C) 2010 S. Karger AG, Basel
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