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Serum Amyloid A Induces Inflammation, Proliferation and Cell Death in Activated Hepatic Stellate Cells

Fig 5

SAA does not signal in HSCs through TLR4, IL-1R, TNF-R1 or SR-BI.

A. Activated human HSCs were pretreated with pertussis toxin followed by treatment with rhSAA (5 μM). Activation of JNK, IKK and Erk pathways was analyzed by immunoblot for p-c-Jun, p-p65 and pErk. B. Activated human HSCs were pretreated with SR-BI blocking antibody or control antibody followed by rhSAA (5 μM) stimulation. JNK activation was analyzed by western blot using phospho-specific antibodies for its substrate c-Jun. C. Skin fibroblasts from TLR4-sufficient C3H/HeOuJ and TRL4-deficient C3H/HeJ mice were stimulated with rhSAA (5 mM), rmTNFα (30 ng/ml) or LPS (100 nM) followed by immunoblot for p-p65. D. Skin fibroblasts from wild-type mice, TNFRI-knockout mice, IL-1 receptor knockout mice and from TNFRI and IL-1 receptor double knockout mice were treated with rhSAA (5 μM), rmIL-1β (5 ng/ml), rmTNFα (30 ng/ml) or irradiated with UV (100 J/m2) Activation of IKK and JNK was determined by western blot analysis for their phosphorylation of their targets p65 and c-Jun, respectively. E. Mouse embryonic fibroblasts from wild type mice, TRAF-2 deficient mice and RIP-1 deficient mice were treated rhSAA (5 μM), rmIL-1β (5 ng/ml), rmTNFa (30 ng/ml) or irradiated with UV (20 J/m2). Activation of IKK and JNK was determined by western blot analysis for their phosphorylation of their targets p65 and c-Jun, respectively.

Fig 5

doi: https://doi.org/10.1371/journal.pone.0150893.g005