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Vitamin C attenuates ERK signalling to inhibit the regulation of collagen production by LL-37 in human dermal fibroblasts

Authors
Park, Hyun JeongOck, Sun MyeongKim, Hee JungPark, Hong JinLee, Young BokChoi, Jung MinCho, Chul SooLee, Jun YoungCho, Baik KeeCho, Dae Ho
Issue Date
Aug-2010
Publisher
WILEY-BLACKWELL
Keywords
ERK; human dermal fibroblasts; LL-37; Vitamin C
Citation
EXPERIMENTAL DERMATOLOGY, v.19, no.8, pp E258 - E264
Journal Title
EXPERIMENTAL DERMATOLOGY
Volume
19
Number
8
Start Page
E258
End Page
E264
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13159
DOI
10.1111/j.1600-0625.2010.01070.x
ISSN
0906-6705
1600-0625
Abstract
Vitamin C is used as an anti-ageing agent because of its collagen enhancing effects. The precise cellular signalling mechanism of vitamin C is not well known. Here, we investigate the profibrotic mechanism of vitamin C against LL-37. Antimicrobial peptide LL-37 decreases collagen expression at mRNA and protein levels in human dermal fibroblasts (HDFs). The ability of LL-37 to inhibit collagen expression is dependent on phosphorylation of extracellular signal-regulated kinase (ERK). HDFs and human keloid fibroblasts were treated with vitamin C followed by 2 h of LL-37 treatment. Collagen mRNA expression and total soluble collagen production inhibited by LL-37 was enhanced by treatment with 0.5 mm vitamin C. Vitamin C also decreased intracellular reactive oxygen intermediates (ROI) levels that were increased by LL-37. Furthermore, the phosphorylation of ERK was analysed by Western blot following treatment with vitamin C and LL-37. Vitamin C turned off phosphorylation of ERK that was induced by LL-37. Ets-1 transcriptional factor, which is involved in the regulation of collagen expression by LL-37, was also inhibited by vitamin C. This study shows that vitamin C enhances collagen production by inhibiting the ERK pathway induced by LL-37.
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