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. 2013 Oct 7;8(10):e76822. doi: 10.1371/journal.pone.0076822

Figure 4. IGF1 and GSK3i stimulate Kitl/KITLG transcription.

Figure 4

Results obtained in murine and human smooth muscle cells (A-E), human LX-2 stellate cells (F-G) and human GIST-T1 cells (H-I) are shown. A, Hoffman modulation contrast image of primary human gastric smooth muscle cells. B, KITLG mRNA (total: soluble+membrane-bound) was readily detectable in primary human smooth muscle cells (passage 3) maintained with Smooth Muscle Growth Medium-2 containing insulin, hFGF-B, hEGF and 5% FBS (Lonza) but not in 24-h growth factor- and serum-deficient basal medium. C, Both IGF1 (100 ng/mL) and the GSK3α/β inhibitor SB415286 (30 µM) stimulated Kitl expression in murine gastric tunica muscularis organotypic cultures (n=3/group). D-E, SB415286 stimulated endogenous Kitl expression in murine primary gastric smooth muscle cells (D; n=3/group) and KITLG transcriptional activity in the same cell type transfected with a KITLG promoter (-2120 bp to +407 bp)-pGL3 luciferase construct (E; n=3/group). IGF1 (100 ng/mL; n=3/group) and SB415286 (30 µM; n=6/group) also increased endogenous KITLG mRNA expression in LX-2 (F) and GIST-T1 cells (H) and stimulated KITLG promoter activity in a time-dependent fashion (LX-2: n=6-9/group; G; GIST-T1: n=3-11/group; I). Groups marked by asterisk are different from the control group, and groups not sharing the same superscript letter are different from each other (P<0.05 by post-hoc multiple comparisons).