- 作者：Falk Rauchfuss ; S ; ro Lambeck ; Ralf A. Claus ; Janina Ullmann ; Thomas Schulz ; Martina Weber ; Katrin Katenkamp ; Reinhard Guthke ; Michael Bauer ; Utz Settmacher
- 关键词：AIFM1 ; apoptosis-inducing factor 1 ; mitochondrial ; AP ; activator protein ; ATF ; activating transcription factor ; ATP6V0E2 ; ATPase H+ transporting V0 subunit e2 ; BCL ; B-cell lymphoma 2 ; CD ; cluster of differentiation ; DAVID ; database for annotation ; visuali
- 刊名：Digestive and Liver Disease
- 出版年：2012
- 出版时间：August, 2012
- 年：2012
- 卷：44
- 期：8
- 页码：681-688
- 全文大小：2067 K
Background
Portal vein embolization is a treatment option to achieve a sufficient future remnant liver volume for patients with central liver tumours requiring an extended resection with an extensive parenchymal loss. However, molecular mechanisms of this intervention are up to now poorly understood. The objective of this prospective pilot study was the characterization of molecular events leading to late hypertrophy of the non-embolized liver tissue in the human liver.Methods
Liver tissue of ten patients was collected before and intraoperatively more than one month after embolization. Investigation of molecular features was performed by pangenomic chips, polymerase chain reaction, immunostaining of proliferation marker Ki-67 and immunofluorescence measurements.
Results
Significantly elevated genes hint towards angiogenesis and signalling by insulin-like growth factor and associated binding proteins. Increased transcript levels of activator protein 1 complex members like c-jun were reflecting potential molecular events of liver growth after embolization. Immunofluorescence data confirmed a predominant upregulation of ¦Â-catenin and c-jun (p < 0.1) supported by Ki-67 (p < 0.05) in the non-embolized liver. In silico analysis of transcriptomic dysplasia and hepatocellular carcinoma data showed divergent signatures compared to embolization.
Conclusions
Our findings indicate a sustained regeneration after portal vein embolization reflected in hyperplasia and angiogenesis in the human liver and provide novel molecular mechanisms of interlobe crosstalk.