Die physiologische Bedeutung der akuten portalen Mehrbelastung als Triggermechanismus der Leberregeneration
The impact of portal hypertension on hepatic growth kinetics and molecular priming events is not clear. Since portal branch ligation is known to cause an analogous regenerative response in the portal hyperperfused lobes to that observed after partial hepatectomy without acute liver tissue loss, comparison of both models allows identification of the role of portal hemodynamic changes on the expression of immediate-early genes such as early growth response-1 (Egr-1) and phosphatase of regenerating liver-1 (PRL-1). Operative procedures were carried out in male Wistar rats. Egr-1- and PRL-1-mRNA expression was assessed by RT-PCR and northern blotting techniques. Growth kinetics were measured by liver weight indices and S-phase-specific mRNA level of H2B histone protein (H2B). Growth patterns were similar in both models with the exception of a faster increase in liver volume and an earlier replicative H2B expression following partial hepatectomy. Egr-1 was specifically induced in non-deprived lobes 1 h following portal branch ligation, and to a higher extent following partial hepatectomy. PRL-1 expression peaked 3 h after partial hepatectomy and portal branch ligation in the non-deprived lobes. In conclusion, portal hemodynamic forces apparently affect the expression of Egr-1 and PRL-1 and may thus represent an important physiological trigger in liver regeneration.
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