Fig. 3

Involvement of the MAPK pathway in LL-37-induced ASC proliferation and migration. a Human ASCs were treated with 20 μg/mL LL-37 for 1, 2, 4, 24, and 48 hr. After cell lysis, the levels of phosphorylated ERK1/2, p38, and JNK were determined by western blot analysis. The levels of total ERK1/2, p38, and JNK were used to confirm equal loading of the cell lysates. LL-37 treatment significantly increased the phosphorylation of ERK1/2, p38, and JNK. b ASCs were pretreated with or without a specific inhibitor of ERK1/2 (PD98059), p38 (SB203580), or JNK (SP600125) for 1 hr and then treated with 20 μg/mL LL-37. EGR1 protein levels in cell lysates were analyzed by an EGR1-specific ELISA. c LL-37-enhanced migration decreased in human ASCs treated with PD98059, SB203580, or SP600125. d LL-37-enhanced ASC proliferation was inhibited by treatment with specific inhibitors of ERK1/2, p38, or JNK (similar to ASC migration). A representative experiment from three independent experiments is shown. Bars represent the mean ± SD. *, P < 0.01 vs. control; ^§, P < 0.01 vs. LL-37-treated ASCs. MAPK mitogen-activated protein kinase, ASCs adipose-derived stromal/stem cells, EGR1 early growth response-1