Massive hepatic apoptosis associated with TGF-β1 activation after Fas ligand treatment of IGF binding protein-1–deficient mice
J. Clin. Invest. Julia I. Leu, et al. 111:129 doi:10.1172/JCI16712 [
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Figure 3Low induction of C/EBPβ and enhanced expression of the major antiapoptotic proteins in
IGFBP-1–/– livers after Fas agonist treatment. (
a) Western blot demonstrating kinetics of C/EBPβ, IGFBP-1, Bcl-2, Bcl-x
L, and AKT induction in Fas agonist–treated
IGFBP-1–/– and
IGFBP-1+/+ livers at the indicated timepoints. (
b–
e) Hematoxylin and eosin stain of (
b)
IGFBP-1+/+ liver 7 hours after treatment with preimmune serum, (
c)
IGFBP-1+/+ liver 7 hours after treatment with anti–IGFBP-1 Ab, (
d)
IGFBP-1+/+ liver 7 hours after treatment with anti-SnoN Ab and Fas agonist, and (
e)
IGFBP-1+/+ liver 7 hours after treatment with anti–IGFBP-1 Ab and Fas agonist. Scale bars: 50 μm. (
f) Western blot analyses comparing induction of AKT, Bcl-2, and caspase-3 processing in
IGFBP-1+/+ livers,
IGFBP-1+/+ and
IGFBP-1–/– livers pretreated with anti–IGFBP-1 Ab, and IGFBP-1–pretreated
IGFBP-1–/– livers after Fas challenge at the indicated timepoints. (
g) Levels of IGFBP-1 detected in whole-cell liver extracts in the indicated animals. α-SnoN, anti-SnoN.
