Fig. 7
GroPIns4P binding to Shp1 facilitates and mediates EGF-induced wound closure in NIH3T3 cell monolayers. a Representative phase-contrast microscopy images after 6 h from scratching in serum-starved NIH3T3 cells untreated (untreated) or treated with 50 μM of GroPIns4P alone (a) or in presence of TPI-1 (b) or NSC-87877 Shp1 inhibitors (c), as indicated. d Quantification of wound healing as the percentage of the untreated control in cells treated as in a-c. e, f Cells without or with pre-incubation with the cPLA2α inhibitor, TPI-1, or NSC-87877 inhibitors (as indicated) were stimulated with 10 ng/ml EGF, 50 μM GroPIns4P or 10 μM arachidonic acid for 6 h. Quantifications of wound healing are presented as the percentage of the untreated controls. The differences between the untreated controls are not statistically significant. Data are expressed as the means (±SE) of at least three independent experiments. ***P < 0.001; **P < 0.02; *P < 0.05 (Student’s t-test) calculated for each treatment versus untreated samples (control). The cPLA2α inhibitor was used at 0.5 μM, but it was effective over a range of concentrations between 0.1 and 2 μM. Arachidonic acid was used at both 10 and 50 μM, with similar results