Lesurtel Mickael, Graf Rolf, Aleil Boris, Walther Diego J, Tian Yinghua, Jochum Wolfram, Gachet Christian, Bader Michael, Clavien Pierre-Alain
Department of Visceral and Transplantation Surgery, University Hospital of Zurich, Switzerland.
Science. 2006 Apr 7;312(5770):104-7. doi: 10.1126/science.1123842.
The liver can regenerate its volume after major tissue loss. In a mouse model of liver regeneration, thrombocytopenia, or impaired platelet activity resulted in the failure to initiate cellular proliferation in the liver. Platelets are major carriers of serotonin in the blood. In thrombocytopenic mice, a serotonin agonist reconstituted liver proliferation. The expression of 5-HT2A and 2B subtype serotonin receptors in the liver increased after hepatectomy. Antagonists of 5-HT2A and 2B receptors inhibited liver regeneration. Liver regeneration was also blunted in mice lacking tryptophan hydroxylase 1, which is the rate-limiting enzyme for the synthesis of peripheral serotonin. This failure of regeneration was rescued by reloading serotonin-free platelets with a serotonin precursor molecule. These results suggest that platelet-derived serotonin is involved in the initiation of liver regeneration.
肝脏在经历重大组织损失后能够再生其体积。在肝脏再生的小鼠模型中,血小板减少或血小板活性受损会导致肝脏无法启动细胞增殖。血小板是血液中血清素的主要载体。在血小板减少的小鼠中,血清素激动剂可恢复肝脏增殖。肝切除术后,肝脏中5-HT2A和2B亚型血清素受体的表达增加。5-HT2A和2B受体的拮抗剂会抑制肝脏再生。在缺乏色氨酸羟化酶1(外周血清素合成的限速酶)的小鼠中,肝脏再生也受到抑制。通过用血清素前体分子重新装载不含血清素的血小板,可挽救这种再生失败的情况。这些结果表明,血小板衍生的血清素参与了肝脏再生的启动过程。