Estrogen and androgen-receptor crosstalk with beta-catenin signaling and sex differences in myocardial hypertrophy
Final Report Abstract
In our approach to understand the role of the ER/β-catenin crosstalk for hypertrophic growth of cardiomyocytes we currently try to establish a test system to quantify hypertrophic growth of HL-1 cells. Using the XCELLigence system, in our first initial studies we observed that treatment of HL-1 cells with endothelin-1 or norepinephrin resulted in a rapid increase in the cell index, which is a measure for the surface area that is occupied by the cells in the wells of the measuring plates. Unfortunately, at the moment this increase in cell size is only detectable for a short period of time, probably because cells were cultivated in the absence of serum before and after stimulation and therefore apparently die within the next hours. We currently try to optimize the conditions and perform additional controls to proof that this increase in cell index indeed represents and corresponds to hypertrophic growth. If these data can be verified, this system will hopefully allow a sensitive, non-invasive, real-time measurement of hypertrophic growth. Further contributions to the research group: In cooperation with Dr. Brozova from Prof. Regitz-Zasgrosek´s group, we generated different PGC1α, MEF2A and MEF2C reporter gene constructs. Furthermore, we provided AC16 cells stably transfected with ER and cells containing a stably integrated ERE-response element. 69 Since only one PhD student position was funded, we decided to focus our work on the crosstalk of ER and β-catenin signaling.
