Cedrol Enhances Extracellular Matrix Production in Dermal Fibroblasts in a MAPK-Dependent Manner

The extracellular matrix (ECM) produced by dermal fibroblasts supports skin structure, and degradation and/or reduced production of ECM are the main causes of wrinkle formation. The aim of this study was to identify the active ingredient that enhances ECM production in dermal fibroblasts. Polarity-b...

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Published inAnnals of dermatology Vol. 24; no. 1; pp. 16 - 21
Main Authors Jin, Mu Hyun, Park, Sun Gyoo, Hwang, Yul-Lye, Lee, Min-Ho, Jeong, Nam-Ji, Roh, Seok-Seon, Lee, Young, Kim, Chang Deok, Lee, Jeung-Hoon
Format Journal Article
LanguageEnglish
Published Korea (South) Korean Dermatological Association; The Korean Society for Investigative Dermatology 01.02.2012
대한피부과학회
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ISSN1013-9087
2005-3894
2005-3894
DOI10.5021/ad.2012.24.1.16

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Summary:The extracellular matrix (ECM) produced by dermal fibroblasts supports skin structure, and degradation and/or reduced production of ECM are the main causes of wrinkle formation. The aim of this study was to identify the active ingredient that enhances ECM production in dermal fibroblasts. Polarity-based fractionation was used to isolate the active ingredient from natural extracts, and the effects of cedrol (isolated from Pterocarpus indicusirginia) on ECM production in cultured human dermal fibroblasts was investigated by reverse transcription-polymerase chain reaction, enzyme linked immunosorbent assay, and Western blot analysis. Cedrol accelerated fibroblast growth in a dose-dependent manner and increased the production of type 1 collagen and elastin. Phosphorylation of p42/44 extracellular signal-regulated kinase, p38 mitogen-activated protein kinase, and Akt was markedly increased by cedrol, indicating that enhanced ECM production is linked to activation of intracellular signaling cascades. These results indicate that cedrol stimulates ECM production, with possible applications to the maintenance of skin texture.
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G704-002233.2012.24.1.005
ISSN:1013-9087
2005-3894
2005-3894
DOI:10.5021/ad.2012.24.1.16