Department of Medical Biology, Akita University Graduate School of Medicine, Akita, 0108543, Japan; Department of Pediatric Surgery, Akita University Graduate School of Medicine, Akita, 0108543, Japan.
Department of Medical Biology, Akita University Graduate School of Medicine, Akita, 0108543, Japan.
Biochem Biophys Res Commun. 2024 Nov 19;734:150632. doi: 10.1016/j.bbrc.2024.150632. Epub 2024 Aug 30.
Hepatic stellate cells (HSCs) are pericytes of the liver responsible for liver fibrosis and cirrhosis, which are the end stages of chronic liver diseases. TGF-β activates HSCs, leading to the differentiation of myofibroblasts in the process of liver fibrosis. While the heterogeneity of HSCs is appreciated in the fibrotic liver, it remains elusive which HSC subsets mainly contribute to fibrosis. Here, we show that the expression of the pericyte marker FoxD1 specifically marks a subset of HSCs in FoxD1-fate tracer mice. HSCs fate-mapped by FoxD1 were preferentially localized in the portal and peripheral areas of both the homeostatic and fibrotic liver induced by carbon tetrachloride. Furthermore, the deletion of Cbfβ, which is necessary for TGF-β signaling, in FoxD1-expressing cells ameliorated liver fibrosis. Thus, we identified an HSC subset that preferentially responds to liver injuries.
肝星状细胞(HSCs)是肝脏的周细胞,负责肝纤维化和肝硬化,这是慢性肝病的终末阶段。TGF-β激活 HSCs,导致肝纤维化过程中肌成纤维细胞的分化。虽然在纤维化的肝脏中已经认识到 HSCs 的异质性,但仍然不清楚哪些 HSC 亚群主要导致纤维化。在这里,我们表明,周细胞标志物 FoxD1 的表达特异性标记 FoxD1 命运追踪小鼠中 HSCs 的一个亚群。FoxD1 标记的 HSCs 优先定位于四氯化碳诱导的稳态和纤维化肝脏的门脉和周边区域。此外,在 FoxD1 表达细胞中敲除 Cbfβ(TGF-β 信号所必需的)可改善肝纤维化。因此,我们鉴定了一个对肝损伤优先反应的 HSC 亚群。