Furthermore, the similar levels of Socs3 and Saa2 induction (downstream STAT3 targets) at 36 hours post PH, suggest that activation of the STAT pathway during the priming phase of PH has occurred normally in mutant livers (Table S3).
A single band of a 64kDa protein was observed from tachyzoite and 6-day post pH shock bradyzoite cultures of parasite lysate probed with tyrosine hydroxylase antibody (Fig. 5B).
Animals were killed at the peak of S-phase (48 h post PH) and after terminated regeneration (96 h post PH).
The inhibitory effect of Sorafenib was transient and restricted to 48 h, but not 96 h post PH.
We demonstrated that Sorafenib already inhibited hepatic S-phase at the peak of DNA replication (48 h post PH) as evidenced by BrdU incorporation analysis.
Animals were killed at 12, 24, 48, or 72 h post-PH, 1 h after injection with [3H]thymidine.
Although TNF was never detected in serum, treatment with anti-TNF pre-PH significantly inhibited increases in serum IL-6 concentration post-PH.
Consistent with the known cAMP stimulation of jun-B in cultured cells, cAMP treatment increased jun-B mRNA, protein, and DNA binding activity post-PH.
PH rapidly increased proliferation of Fn14 cells; hepatocytic cells that expressed Fn14 and other progenitor markers, such as Lgr5, progressively accumulated from 12-8 h post-PH and then declined to baseline by 96 h.
When TWEAK/Fn14 signaling was disrupted, progenitor accumulation, induction of pro-regenerative cytokines, hepatocyte and cholangiocyte proliferation, and over-all survival were inhibited, while post-PH liver damage and bilirubin levels were increased.
