THE TRANSCRIPTION FACTOR c-JUN/ AP-1 PROMOTES

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Suppl. Figure Legends
Suppl. Figure S1
(A) Hepatic c-Jun expression in mice with the indicated genotypes was analyzed at 3,
6 and 12 months of age by immunoblotting. (B) Hepatic c-Jun expression is induced
following infection with AdenoHBV in a mouse model of HBV infection, as compared
to mice infected with control adenovirus, as determined by immunohistochemistry.
(C) Expression of HBV transgenes was analyzed by ELISA in serum and total liver
lysates of mice with the indicated genotypes at 6 months of age (n = 3-4/genotype) or
by immunoblotting of LHBs antigen. (D) Expression of HBsAg was analyzed in mice
of the indicated genotypes at 12 months of age by immunohistochemistry.
Suppl. Figure S2
(A) Infiltration of CD3+ T-cells and Ly6G+ neutrophils was analyzed by
immunohistochemistry. 4 mice/genotype were analyzed and positive cells were
counted in four 200x power fields, each. Mean cell numbers/mouse are given. (B)
Expression
of
c-Jun
in
HBV-related
pathologies
as
determined
by
immunohistochemistry.
Suppl. Figure S3
Expression of ER stress-related genes, Birc5 as well as Stat3 signaling are not
affected in the absence of c-Jun. (A) Hepatic expression of ER stress related genes,
Birc5 and genes related to oxidative stress in mice with the indicated genotypes at 6
and 12 months of age, respectively, as determined by qPCR. (B) Western blot
analysis of the indicated proteins in total liver lysates of 12 months old mice with the
indicated genotypes.
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Suppl. Figure S4
TUNEL stainings of mouse livers with the indicated genotypes were performed at 6
months of age. ConA-treated control mice were used as positive controls (TUNEL
positive hepatocytes are indicated by white arrows).
Suppl. Figure S5
c-Jun interferes with expression of p21 and Opn in a cell autonomous manner in vitro
and
regulates
Opn
expression
during
T-cell
mediated
hepatitis
in
vivo.
(A) Hepatic p21 expression was assessed by immunohistochemistry at 6 months of
age. For quantification, 3 representative high power fields were analyzed per mouse.
(n = 3/genotype; normal distribution assumed). (B) Expression of the indicated genes
was analyzed in HBV+ c-Junf/f PMH following adenoviral transfer of Cre recombinase
or GFP. (n = 8/group, significance was tested by TT). (C) Hepatic Opn expression
was determined in mice treated with ConA (10mg/kg, analysis after 4h). (n =
4/genotype; significance was tested by MWT).
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