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Additional Supporting Information may be found in the online version of this article.

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HEP_26069_sm_SuppFig1.tif1468KSupplementary Figure 1: Densitometric quantification of p-Akt/Akt ratio in CXCL10 treated hepatocytes within 60 min (A) and within 8 hours (B). *P<0.05, **P<0.01, ***P<0.001. Data are normalized to vehicle-treated control and are expressed as means ± SEM of three independent experiments.
HEP_26069_sm_SuppFig2.tif1590KSupplementary Figure 2: Densitometric quantification of p-JNK/JNK, cleaved Casp3/β-actin and PAK-2p34/PAK-2 ratio in CXCL10 treated hepatocytes (A). Densitometric quantification of p-Akt/Akt, p-JNK/JNK, cleaved Casp3/β-actin and PAK-2p34/PAK-2 ratio in CXCL10 and Wortmannin treated hepatocytes (B). *P<0.05, **P<0.01, ***P<0.001. Data are normalized to vehicle-treated control and are expressed as means ± SEM of three independent experiments.
HEP_26069_sm_SuppFig3.tif1568KSupplementary Figure 3: Densitometric quantification of p-Akt/Akt, p-JNK/JNK, cleaved Casp3/β-actin and PAK-2p34/PAK-2 ratio in CXCL10 treated Casp8-/- hepatocytes (A). Densitometric quantification of p-Akt/Akt ratio in CXCL10 treated CXCR3-/- hepatocytes (B). Potential LPS contamination of the recombinant CXCL10 was further assessed by preincubation of CXCL10 with polymyxin B, which inhibits LPS. This preparation did not change CXCL10-mediated Caspase-3 (C) and Akt activation (D). *P<0.05, **P<0.01, ***P<0.001. Data are normalized to vehicle-treated control and are expressed as means ± SEM of three independent experiments.
HEP_26069_sm_SuppFig4.tif1577KSupplementary Figure 4: Expression of TLR4 on hepatocytes by RT-PCR. 18s was used as reference gene. Control, water (A). Densitometric quantification of p-Akt/Akt ratio in CXCL10 treated TLR4-/- hepatocytes (B). The apoptotic response in Cxcl10 treated wild-type and TLR4-/- mice was also reflected by strongly increased hepatic Caspase-8 activity (C). *P<0.05.
HEP_26069_sm_SuppFig5.tif1106KSupplementary Figure 5: Proposed CXCL10-induced pathway in hepatocytes Through TLR4, CXCL10 activates PI3K and induces long-term Akt and JNK phosphorylation. Sustained phosphorylation of JNK leads to Caspase-8 and Caspase-3 activation, followed by PAK-2 cleavage. PAK-2p34 fragment translocates to the nucleus and induces apoptosis pathways, while constitutively active (non-cleaved) PAK-2 has been implicated in survival pathways.

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