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Media type:
E-Book;
Thesis
Title:
Funktionen des Transkriptionsfaktors c-Jun in der ER-Stressantwort der Leber
Other titles:
abweichender Titel: Übers. des Hauptsacht.: Functions of the transcription factor c-Jun in the hepatic ER-stress response
Übers. des Hauptsacht.: Functions of the transcription factor c-Jun in the hepatic ER-stress response
University thesis:
Freiburg i. Br., Univ., Diss., 2011
Footnote:
Description:
Zusammenfassung: Introduction: The accumulation of proteins in the endoplasmic reticulum (ER) and the triggered cellular ER-stress response are associated with cell damage in a wide range of liver diseases. However, the involved signaling pathways have not yet been adequately characterized. Preliminary work has shown that the transcription factor c-Jun/AP-1 posseses important functions in the regulation of survival and proliferation of hepatocytes in acute hepatitis and liver cancer. Objectives: Therefore, here we investigated the functions of c-Jun in the ER-stress response of the liver. Methods: ER-stress was induced in human hepatoma cells either through the chemical ER-stressors Thapsigargin and Tunicamycin or by the expression of hepatoviral proteins. The functions of c-Jun were then determined through RNAi. In addition ER-stress was chemically induced in liver specific conditional c-Jun knockout-mice. Results: In hepatoma cells the induction of ER stress resulted in a rapid and significant expression of c-Jun. Surprisingly, the inhibition of c-Jun expression by RNAi had no effect on cell survival. Primary mouse hepatocytes, however, showed an exacerbation of ER-stress, a vacuolisation of the cytoplasm, a decrease in cell survival and an increased expression of proinflammatory cytokines in the absence of c-Jun. Conclusion: In summary this data shows a protective effect of c-Jun in the context of the ER-stress response and a reduction in the inflammatory response in liver cells under ER-stress conditions by c-Jun