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. 2014 Jul 25;155(10):3956–3969. doi: 10.1210/en.2013-2095

Figure 2.

Figure 2.

Effects of ghrelin on leptin-stimulated STAT3 and JAK2 phosphorylation in cultured rat NG neurons. A, Leptin (Lep, 1nM) caused a 2.52 ± 0.35–fold increase in STAT3 phosphorylation, which was significantly inhibited (> 65%) by ghrelin (10nM, Ghr). B, Leptin (1nM) caused a 1.92 ± 0.24–fold increase in JAK2 phosphorylation, which was significantly inhibited (> 80%) by ghrelin (10nM). C, Leptin (10nM) caused a significant (2.48 ± 0.33–fold) increase in PI3K phosphorylation and a significant (3.19 ± 0.27–fold) increase in MAPK phosphorylation (panel D), which was significantly inhibited by ghrelin (10nM) in both studies. The data are representative of five independent experiments. *, P < .05 significantly different from unstimulated control; **, P < .05, significantly different from leptin-stimulated STAT3, JAK2, PI3K, or MAPK phosphorylation. E, Ghrelin-stimulated SOCS3 expression in a dose-dependent manner. NG neurons were stimulated with ghrelin (0–100nM) for 60 minutes. SOCS3 expression was significantly increased at 10, 20, and 50nM. F, Similarly, ghrelin (10 and 20nM) significantly stimulated Epac1 expression. The data are representative of five independent experiments. *, P < .05 suggests statistical significance from unstimulated control.