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. 2012 Sep 13;61(10):2609–2620. doi: 10.2337/db11-1415

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© 2012 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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FIG. 2. — Inhibition of macrophage MEK signaling induces the UPR and promotes ER stress–associated apoptosis. A and B: Concanavalin A–elicited peritoneal WT macrophages were treated with inhibitors of PI3K (LY294002 [LY], 10 μmol/L), MEK (PD98059 or U0126, 10 μmol/L), mammalian target of rapamycin (rapamycin [Rapa], 2 μmol/L), protein kinase C (GF109203 [GF], 2 μmol/L), or palmitic acid–BSA (PA-BSA, 0.5 mmol/L) in DMEM with 10% FBS for 12 h. Protein lysate of macrophages treated with thapsigargin (Thap, 5 μmol/L) or tunicamycin (Tuni, 2.5 μg/mL) was used as positive controls. The levels of indicated proteins were determined by Western analysis. Data represent mean ± SEM. n = 3. *P < 0.05. C: Concanavalin A–elicited peritoneal macrophages isolated from Insr^+/+ and Insr^−/− mice were treated with or without AcLDL (100 μg/mL) + 58-035 (10 μg/mL) for 5 h. The expression of P-ERK, ERK, P-AKT, and AKT was determined by Western analysis. n = 3. D: WT peritoneal macrophages pretreated with or without the inhibitors of MEK (U0126 or PD98059) were incubated with or without AcLDL (100 μg/mL) and compound 58035 (10 μg/mL) or 7-ketocholesterol (40 μg/mL) at 37°C for ∼8 h. Apoptosis of macrophages was determined by annexin V staining. n = 3. *P < 0.05 for free cholesterol–loaded cells with vs. without the treatment of U0126 or PD98059 compounds. E and F: Concanavalin A–elicited peritoneal macrophages isolated from Insr^+/+ (WT) and Insr^−/− mice were infected with adenovirus either harboring lacZ (Ad-LacZ) or constitutively active MEK mutant (Ad-MEK) for ∼30 h. Macrophage protein extracts

FIG. 2. — Inhibition of macrophage MEK signaling induces the UPR and promotes ER stress–associated apoptosis. A and B: Concanavalin A–elicited peritoneal WT macrophages were treated with inhibitors of PI3K (LY294002 [LY], 10 μmol/L), MEK (PD98059 or U0126, 10 μmol/L), mammalian target of rapamycin (rapamycin [Rapa], 2 μmol/L), protein kinase C (GF109203 [GF], 2 μmol/L), or palmitic acid–BSA (PA-BSA, 0.5 mmol/L) in DMEM with 10% FBS for 12 h. Protein lysate of macrophages treated with thapsigargin (Thap, 5 μmol/L) or tunicamycin (Tuni, 2.5 μg/mL) was used as positive controls. The levels of indicated proteins were determined by Western analysis. Data represent mean ± SEM. n = 3. *P < 0.05. C: Concanavalin A–elicited peritoneal macrophages isolated from Insr^+/+ and Insr^−/− mice were treated with or without AcLDL (100 μg/mL) + 58-035 (10 μg/mL) for 5 h. The expression of P-ERK, ERK, P-AKT, and AKT was determined by Western analysis. n = 3. D: WT peritoneal macrophages pretreated with or without the inhibitors of MEK (U0126 or PD98059) were incubated with or without AcLDL (100 μg/mL) and compound 58035 (10 μg/mL) or 7-ketocholesterol (40 μg/mL) at 37°C for ∼8 h. Apoptosis of macrophages was determined by annexin V staining. n = 3. *P < 0.05 for free cholesterol–loaded cells with vs. without the treatment of U0126 or PD98059 compounds. E and F: Concanavalin A–elicited peritoneal macrophages isolated from Insr^+/+ (WT) and Insr^−/− mice were infected with adenovirus either harboring lacZ (Ad-LacZ) or constitutively active MEK mutant (Ad-MEK) for ∼30 h. Macrophage protein extracts