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. 2014 Nov 18;4:7096. doi: 10.1038/srep07096

Figure 3. Involvement of PI3K in the leptin-induced expression of GRP78.

Figure 3

(A). SH-SY5Y-ObRb cells were pretreated with PD98059 (PD; 10 μM) or LY294002 (LY; 5 μM) for 30 min followed by leptin (0.5 μg/ml, 30 min). Western blotting analysis was performed using specific antibodies for phospho-Akt (Thr308), Akt, phospho-ERK 1/2 (Thr202/Tyr204), ERK, phospho-STAT3 (Tyr705), STAT3, and GAPDH. (B). Densitometric analysis of phospho-Akt (Thr308), phospho-ERK1/2 (Thr202/Tyr204), and phospho-STAT3 (Tyr705) levels using image analyzing software. The treatment with PD inhibited the phosphorylation of ERK, but not Akt. The treatment with LY significantly inhibited the phosphorylation of Akt and also slightly inhibited that of ERK. The treatment with PD or LY did not inhibit the phosphorylation of STAT3. Data are expressed as the mean ± S.E. of 3 independent experiments (n = 3). ** P < 0.01. (C). SH-SY5Y-ObRb cells were pretreated with PD98059 (PD; 10 μM) or LY294002 (LY; 5 μM) for 30 min followed by leptin (0.5 μg/ml, 24 h). Western blotting analysis was performed using antibodies for GRP78 and GAPDH. (D). A densitometric analysis of GRP78 levels were performed using image analyzing software. LY hindered the effects of leptin on the induction of GRP78 expression. Data are expressed as the mean ± S.E. of 4 independent experiments (n = 4). ** P < 0.01.