Tacke Frank, Trautwein Christian, Zhao Shourong, Andreeff Michael, Manns Michael P, Ganser Arnold, Schöffski Patrick
Department of Gastroenterology and Hepatology, Hannover Medical School, Carl-Neuberg-Strasse 1, D-30625 Hannover, Germany.
Liver. 2002 Jun;22(3):205-12. doi: 10.1034/j.1600-0676.2002.01642.x.
BACKGROUND/AIMS: Platelet production is regulated by thrombopoietin (TPO), which is primarily synthesized in the liver. The TPO in patients with liver diseases could possibly be owing to impaired hepatic TPO production. As we reported previously, TPO serum levels are not decreased in patients with liver diseases compared with healthy controls and do not depend on the stage of cirrhosis or platelet count, but are highly elevated in patients with chronic virus hepatitis.
To study possible mechanisms, we measured hepatic TPO mRNA levels in liver tissue samples from 31 liver cirrhosis patients by quantitative TaqMan real-time RT-PCR and corresponding serum TPO concentrations by ELISA.
Median TPO serum levels were elevated in patients with viral hepatitis (n = 12) compared with patients with a biliary (n = 10), alcoholic (n = 6) or other (n = 3) disease etiology, while hepatic TPO mRNA levels did not differ. The TPO mRNA levels in patients with chronic liver diseases were not different from normal liver tissue sample. The TPO mRNA and TPO serum level did not correlate.
We conclude that hepatic TPO gene expression appears to be maintained on a constitutive transcriptional level in patients with liver diseases and does not change dependent on disease etiology.
背景/目的:血小板生成受血小板生成素(TPO)调节,TPO主要在肝脏合成。肝病患者体内的TPO可能是由于肝脏TPO生成受损。正如我们之前报道的,与健康对照相比,肝病患者的血清TPO水平并未降低,且不依赖于肝硬化阶段或血小板计数,但在慢性病毒性肝炎患者中会显著升高。
为研究可能的机制,我们通过定量TaqMan实时逆转录聚合酶链反应(RT-PCR)检测了31例肝硬化患者肝组织样本中的肝脏TPO mRNA水平,并通过酶联免疫吸附测定(ELISA)检测了相应的血清TPO浓度。
与胆汁淤积性(n = 10)、酒精性(n = 6)或其他病因(n = 3)的患者相比,病毒性肝炎患者(n = 12)的血清TPO中位数水平升高,而肝脏TPO mRNA水平无差异。慢性肝病患者的TPO mRNA水平与正常肝组织样本无差异。TPO mRNA与血清TPO水平不相关。
我们得出结论,肝病患者肝脏TPO基因表达似乎在组成型转录水平上维持,且不随疾病病因改变。