Sinusoidal endothelial cells coordinate liver regeneration and angiogenesis via angiopoietin-2: an ode to prometheus.
Sinusoidal endothelial cells coordinate liver regeneration and angiogenesis via angiopoietin-2: an ode to prometheus.
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DOI：
10.1053/j.gastro.2014.06.015
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发表时间：
2014-08
期刊：
影响因子：
29.4
通讯作者：
Ruisi Wang;R. Huebert;V. Shah
中科院分区：
文献类型：
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作者：
Ruisi Wang;R. Huebert;V. Shah
2014 年 8 月 精选摘要 533 通过去除 TGF-b1“刹车”实现肝细胞增殖。一种不同的机制解释了 Ang-2 对肝再生后期血管生成阶段的刺激作用，即 Ang-2 通过自分泌刺激 Ang-2 受体 Tie2 上调血管内皮生长因子受体 2 (VEGFR-2)。作者得出结论，LSEC 不仅对分泌的信号做出反应，而且还产生直接调节肝再生的信号。在 PHx 后的早期阶段，LSEC 衍生的 Ang-2 下调，导致 TGF-b1 减少，并允许肝细胞增殖。在血管生成阶段，Ang-2 上调会激发 VEGFR-2 信号传导，从而诱导非实质细胞增殖。因此，单个分子 Ang-2 可以通过时间和细胞类型特异性效应来调节肝再生。
August 2014 Selected Summaries 533 hepatocyte proliferation by removing the TGF-b1 “brake.” A different mechanism accounted for the stimulatory effects of Ang-2 on the later angiogenic phase of liver regeneration whereby Ang-2 up-regulates vascular endothelial growth factor receptor-2 (VEGFR-2) through autocrine stimulation of the Ang-2 receptor, Tie2.The authors conclude that LSEC not only respond to secreted signals, but also generate signals to directly modulate liver regeneration. In the early phase after PHx, LSEC-derived Ang-2 is down-regulated, resulting in reduced TGF-b1, and allowing hepatocyte proliferation. In the angiogenic phase, Ang-2 up-regulation provokes VEGFR-2 signaling to induce proliferation of nonparenchymal cells. Thus, a single molecule, Ang-2, can regulate liver regeneration through temporal and cell-type–specific effects.