MEK/Erk1/2 Signaling Is Involved in SLC37A2-Mediated Inflammation
(A and B) BMDMs from WT and Slc37a2−/− mice were treated with 100 ng/mL LPS for 0–6 h. Cell lysates were used for immunoblotting signal molecules in MAPK and NF-κB pathways (A) and PI3K/Akt1, mTORC1, and mTORC2 pathways (B). The intensity of each target protein band was normalized to its total (unphosphorylated) form or β-actin. The intensity of WT macrophage protein band at 0 h was set to 1; the intensity of each protein band relative to the WT control macrophages at 0 h is then calculated. The results are representative of two independent experiments. The average of the densitometry of the two experiments was shown under each protein band.
(C–E) Secretion of cytokines from WT and Slc37a2−/− BMDMs pretreated with IκBα inhibitor Bay 11-7082 (Bay11, 5 μM), p38 MAPK inhibitor III (p38i, 2 μM), MEK/Erk1/2 inhibitor U0126 (25 μM), PI3K inhibitor Ly294002 (20 μM), mTOR inhibitors rapamycin (50 nM), and Torin 1 (100 nM), followed by 100 ng/mL LPS for 6 h in the presence of inhibitors.
Data are representative of two independent experiments with 4 samples per group (mean ± SEM). ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.001, unpaired, two-tailed Student's t test.