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

• Published in: Pharmacology Vol. 85; no. 2; pp. 68 - 76
• Main Authors: Kim, Won-Serk, Yang, You Jin, Min, Hyung Geun, Song, Min Gyu, Lee, Ji-Seon, Park, Keung-Young, Kim, Jin-Ju, Sung, Jong-Hyuk, Choi, Jun-Seok, Cha, Hyuk-Jin
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland S. Karger AG 01.01.2010
• Subjects: Administration, Topical; Animals; Cells, Cultured; Enzyme Activation - drug effects; Enzyme Activation - physiology; Female; Fibroblasts - drug effects; Fibroblasts - enzymology; Humans; MAP Kinase Signaling System - drug effects; MAP Kinase Signaling System - physiology; Mice; Mitogen-Activated Protein Kinase 1 - metabolism; Mitogen-Activated Protein Kinase 1 - physiology; Mitogen-Activated Protein Kinase 3 - metabolism; Mitogen-Activated Protein Kinase 3 - physiology; Original Paper; Rats; Rats, Hairless; Skin - cytology; Skin - drug effects; Skin - enzymology; Sulfonium Compounds - administration & dosage; Time Factors; Vitamin U - administration & dosage; Wound Healing - drug effects; Wound Healing - physiology; ERK1/2 pathway; Wound healing; Proliferation; S-methylmethionine sulfonium; Migration
• ISSN: 0031-7012; 1423-0313
• DOI: 10.1159/000276495

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.