Extracellular matrix gene expression altered by N-methylethanolamine (MEA) in human dermal fibroblasts / Japan Scar Workshop


Papers of The 1st Japan Scar Workshop
7. Extracellular matrix gene expression altered by N-methylethanolamine (MEA) in human dermal fibroblasts Yamanaka M, Ishikawa O Department of Dermatology, Gunma University Graduate School of Medicine, Gunma, Japan
Tissue fibrosis develops when dysregulation of extracellular matrix (ECM) turnover favors deposition of ECM proteins over degradation. Fibrosis may then lead to organ dysfunction as observed in keloids and hypertrophic scars. In the present study, we investigated the antifibrotic properties of N-methylethanolamine (MEA). MEA suppressed the expression of COL2(I) mRNA and its protein levels in a dose- and time-dependent manner in human dermal fibroblasts. Under the same conditions, MEA enhanced the expression of matrix metalloproteinase-1 (MMP-1) mRNA and its protein levels. Together, these observations suggest that MEA may inhibit ECM deposition . We investigated which pathway is involved in the action of MEA. We focused on the MEK/ERK signaling pathways. Assays using specific inhibitors of MEK/ERK pathways, PD98059 and U0126, indicated that the MEK/ERK pathways are involved in MEA-induced MMP1 stimulation and COL2(I) inhibition. We confirmed that MEA induced ERK1/2 phosphorylation. In conclusion, our study demonstrates that MEA displays an antifibrotic action by reducing type-I collagen production and inducing MMP-1 production. Therefore, MEA can be a promising candidate for the treatment of diseases characterized by excessive ECM deposition such as keloids and hypertrophic scars.
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