Detailed Instructions: Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.
Problem:Context: The role of signal transducer and activator of transcription 3 (Stat3) in liver fibrosis is still controversial. Since hepatic stellate cells (HSCs) and transforming growth factor-1 (TGF-1) are central to the fibrogenesis, our goal was to clarify the mechanism of Stat3 crosslinking of TGF-1 signaling.', 'Stat3, TGF-1 mRNA and protein expressions were examined in liver tissues of chronic hepatitis B (CHB) patients and diethylinitrosamine (DEN)-induced rat fibrosis model. The effect of Stat3 activation or suppression on TGF-1 signaling in HSCs was tested in vitro and in vivo.', 'Stat3 expression as well as TGF-1 was increased in CHB patients and DEN-induced fibrosis rat model. This was strongly correlated with increase in fibrosis staging. TGF-1, a mediator of fibrosis, was enhanced by Stat3, but suppressed by siRNA-mediated RNA knockdown of Stat3 (siStat3) or Janus kinase 2 inhibitor (AG490) both in vivo and in vitro. Stat3 crosslinking TGF-1 signaling plays an important role in HSC activation and increasing fibrosis related products. TGF-1 could not achieve profibrogenic cytokine and anti-apoptosis characteristics without Stat3 activation in HSCs.
Answer: We provide a novel role of Stat3 cooperating TGF-1 in activation and anti-apoptotic effect of HSCs. Stat3 worsens liver fibrosis through the up-regulation of TGF-1 and fibrotic product expression.
Solution:
Does stat3 signaling activation crosslinking of TGF-1 in hepatic stellate cell exacerbate liver injury and fibrosis?