Hung, Chi-Feng Hsiao, Chien-Yu Hsieh, Wen-Hao Li, Hsin-Ju Tsai, Yi-Ju Lin, Chun-Nan Chang, Hsun-Hsien Wu, Nan-Lin 18β-GA-d increased the phosphorylation of Akt, ERK1/2, and p38 in human dermal fibroblasts. <p>(A) Human dermal fibroblasts were treated with 0.1% THF or 18β-GA-d (30 μM) for different times. The level of phosphorylation of Akt, ERK1/2, and p38 at different times was analyzed by western blot assay. The quantification data for the ratios of phosphorylated protein/total non-phosphorylated protein in THF- and 18β-GA-d- treated groups to those in the untreated groups are shown in the lower panels. *<i>p</i> < 0.05 compared with THF treatment at the same time point (mean ± S.E.M. n = 3). (B) Human dermal fibroblasts were pretreated with UO126 (ERK inhibitor) (20 μM), MK2206 (Akt inhibitor) (5 μM), or SB203580 (p38 inhibitor) (10 μM) and then treated with 0.1% THF or 18β-GA-d (30μM) for 24 h. The protein expression of AQP-3 was evaluated by western blot assay. The quantification data for ratios of AQP-3/α-tubulin in different groups, relative to AQP-3/α-tubulin in the THF-treated group, are shown in the right panel. *<i>p</i> < 0.05 (mean ± S.E.M. n = 3).</p> HaCaT keratinocytes;18β- GA derivative-induced expression;migration;18β- GA;role;aquaporin -3 expression;aquaporin -3;proliferation;fibroblast;compound;scratch wound healing assay;ERK;cause cell death 2017-08-16
    https://plos.figshare.com/articles/figure/18_-GA-d_increased_the_phosphorylation_of_Akt_ERK1_2_and_p38_in_human_dermal_fibroblasts_/5315833
10.1371/journal.pone.0182981.g005