Lipopolysaccharide Inhibits Autophagy and Promotes Inflammatory Responses via p38 MAPK-Induced Proteasomal Degradation of Atg13 in Hepatic Stellate Cells

<div>LPS promotes depletion of Atg13 and inflammatory responses in LX2 cells. LPS (1 μg/mL, 0-16 h) suppressed expression of Atg13 in a time-dependent manner. (c) LPS (0-3 μg/mL, 4 h) suppressed expression of Atg13 in a dose-dependent manner. (a, b) LPS (1 μg/mL, 0-16 h) activated NLRP3 inflammasome activation and IL-1β secretion in a time-dependent manner. (d) LPS (1 μg/mL, 0-4 h) did not alter the expression of Atg13 in HL-7702 cells. (e) LPS (1 μg/mL, 0-16) did not alter the mRNA levels of Atg13 in LX2 cells.</div>

Mediators of Inflammation

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Figure 5

Figure 5: Lipopolysaccharide Inhibits Autophagy and Promotes Inflammatory Responses via p38 MAPK-Induced Proteasomal Degradation of Atg13 in Hepatic Stellate Cells 

Figure 5 | Lipopolysaccharide Inhibits Autophagy and Promotes Inflammatory Responses via p38 MAPK-Induced Proteasomal Degradation of Atg13 in Hepatic Stellate Cells 