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Fig. 2 | Molecular Medicine

Fig. 2

From: Vascular smooth muscle cells in response to cholesterol crystals modulates inflammatory cytokines release and promotes neutrophil extracellular trap formation

Fig. 2

CC uptake mechanism in VSMCs. A VSMCs were pre-incubated with DMSO (vehicle, Veh), NF-κB inhibitor BAY 11–7082 (5 μM), cathepsin B inhibitor CA074 (100 μM), ERK1/2 inhibitor PD98059 (10 μM), JAK inhibitor CP690550 (10 μM), AKT inhibitor MK-2206 (1 μM), mTOR inhibitor Ridaforolimus (1 μM), PI3K inhibitor Wortmannin (1 μM), p38 MAPK inhibitor SB203580 (10 μM), serine protease inhibitor 3,4-Dichloroisocoumarin (DCI, 100 μM), and actin inhibitor Cytochalasin D for 1 h prior to CC treatment for 24 h to screen the signaling pathway. B Representative western blot bands showing the expression of PI3K and its downstream proteins in response to CC and wortmannin. The densitometry analysis of significantly altered proteins is shown on right side of the blots. Dose dependent response of PI3K inhibitor (wortmannin) (C), cholesterol binding protein, filipin (D), dynamin GTPase activity inhibitor, dynasore (E), and calcium sensing receptor inhibitor, NPS (F) for 1 h prior to CC uptake in VSMCs. Data are representative of experiments from VSMCs of 4 donors and displayed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001

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