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Fig. 2. (A) Parental and clone-4 cells stained with hematoxylin-eosin before (a,b) and after (c,d) 48 hours of treatment with 10 µM RA. Notice the more differentiated neuronal phenotype acquired by clone-4 cells after such a short exposure to RA (d). (B) Effects of RA exposure on neurite length in parental and clone-4 cells. Notice the large increase in neurite length with 2 days of exposure to RA in clone-4 and parental cells co-treated with RA and 200 µM DETA-NONOate. Bars are the mean±s.e.m. from measuring neurite extension of at least 150 cells per dish in three separate dishes. (C, left) In parallel to stimulation of clone-4 differentiation, RA also slowed down cell proliferation in this clone compared with parental cells, an effect completely reversed by blocking NOS activity using L-NAME (1-5 mM) or the guanylate cyclase inhibitor ODQ (50 µM). (C, right) Inhibition of BrdU incorporation in SK-N-BE cells by RA and DETA-NONOate (50-200 µM) or 8Br-cGMP (250 µM). The antiproliferative effects were determined after treating the parental and clone-4 cells for 2 days with 10 µM RA and labeling with BrdU (10 µM) for the last 2 hours. Results are expressed as the percentage BrdU incorporation relative to parental cells treated with RA. Bars are the mean±s.e.m. of four experiments. *, P<0.01 compared with control cultures; #, P<0.01 compared with clone 4 (Bonferroni's test after ANOVA).
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