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首页> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >Interplay of hepatic and myeloid signal transducer and activator of transcription 3 in facilitating liver regeneration via tempering innate immunity.
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Interplay of hepatic and myeloid signal transducer and activator of transcription 3 in facilitating liver regeneration via tempering innate immunity.

机译：肝和髓样信号转导子与转录激活子3之间的相互作用，通过调节先天免疫力促进肝脏再生。

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摘要

Liver regeneration triggered by two-thirds partial hepatectomy is accompanied by elevated hepatic levels of endotoxin, which contributes to the regenerative process, but liver inflammation and apoptosis remain paradoxically limited. Here, we show that signal transducer and activator of transcription 3 (STAT3), an important anti-inflammatory signal, is activated in myeloid cells after partial hepatectomy and its conditional deletion results in an enhanced inflammatory response. Surprisingly, this is accompanied by an improved rather than impaired regenerative response with increased hepatic STAT3 activation, which may contribute to the enhanced liver regeneration. Indeed, conditional deletion of STAT3 in both hepatocytes and myeloid cells results in elevated activation of STAT1 and apoptosis of hepatocytes, and a dramatic reduction in survival after partial hepatectomy, whereas additional global deletion of STAT1 protects against these effects. Conclusion: An interplay of myeloid and hepatic STAT3 signaling is essential to prevent liver failure during liver regeneration through tempering a strong innate inflammatory response mediated by STAT1 signaling.
机译：三分之二的部分肝切除术引发的肝再生伴随着肝内毒素水平的升高，这有助于再生过程，但肝脏炎症和细胞凋亡仍然矛盾地受到限制。在这里，我们显示部分肝切除术后骨髓细胞中信号转导和转录激活因子3（STAT3）（一种重要的抗炎信号）被激活，其条件性缺失导致炎症反应增强。出人意料的是，伴随着肝STAT3活化的增加，再生反应得到改善而不是受损，这可以促进肝脏再生。实际上，肝细胞和髓样细胞中STAT3的条件缺失都会导致STAT1的活化增强和肝细胞凋亡，并且在部分肝切除术后生存率急剧下降，而STAT1的其他整体缺失则可以防止这些作用。结论：骨髓和肝STAT3信号的相互作用对于通过调节由STAT1信号介导的强烈的先天性炎症反应来预防肝再生期间的肝衰竭至关重要。

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