Figure 5

Intracellular FGF1 does not protect N2a cells from p53-dependent apoptosis. (a) N2a cells were transiently co-transfected with GFP and FGF1^WT or empty (mock) expression vectors and then treated or not with etoposide for 24 h. Following transfection and treatment, N2a transfected apoptotic cells were quantified by flow cytometry after CMX-Ros staining. Transfected apoptotic cells correspond to the high GFP (transfected cells, GFP+), low CMX-Ros (low ΔΨm, CMX−) and small-sized (size−) cells. The graph represents the mean±S.E.M. of three independent experiments. Student’s t-tests were performed relative to the control Mock cells, except where indicated (n=3; n.s.: P>0.05; **: P⩽0.01). (b) N2a cells were transiently transfected with FGF1^WT or empty (mock) expression vectors and then treated or not with etoposide for 24 h. FGF1 expression, p53 activation (Ser15 phosphorylation) and caspase-3 cleavage were analyzed by western blot. Actin detection was used as a control