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. 2009 Jun;156(3):413–418. doi: 10.1111/j.1365-2249.2009.03915.x

Fig. 4.

Fig. 4

CXCL16 induced human gingival fibroblasts (HGF) proliferation and extracellular regulated kinase (ERK) and protein kinase B (AKT) phosphorylation. (a) HGF were treated with or without CXCL16 (1, 10 or 100 ng/ml) for 24 h. Cell proliferation was assessed using TetraColor One assay. Data are representative of HGF from three different donors. The results were calculated as the mean and standard deviation (s.d.) of one representative experiment performed in triplicate. Error bars show the s.d. of the values. *P < 0·05; **P < 0·01 significantly different from the median. (b) HGF were stimulated with CXCL16 (100 ng/ml) for 5, 15, 30 or 60 min. Extracts were electrophoresed and blotted with phosphor-ERK, total ERK, phospho-AKT or total AKT antibodies. (c) HGF were preincubated with PD98059 (20 µM) or LY294002 (20 µM) for 1 h and then incubated with CXCL16 (100 ng/ml) for 24 h. Cell proliferation was assessed using TetraColor One assay. Data are representative of HGF from three different donors. The results were calculated as the mean and s.d. of one representative experiment performed in triplicate. Error bars show the s.d. of the values. *P < 0·05; **P < 0·01 significantly different from CXCL16-treated HGF without inhibitors.