BioProject

C57BL/6N animals received at the age of 6 weeks either adeno associated virus from serotype 9 (AAV9) leading to cardiac overexpression of luciferase (Luc, as control) or amino acids 1-201 of histone deacetyase 4 (HDAC4-NT) under the control of the cardiac myocyte-specific CMV-enhanced short (260bp) myosin light chain promoter (CMVenh/MLC260). More...

C57BL/6N animals received at the age of 6 weeks either adeno associated virus from serotype 9 (AAV9) leading to cardiac overexpression of luciferase (Luc, as control) or amino acids 1-201 of histone deacetyase 4 (HDAC4-NT) under the control of the cardiac myocyte-specific CMV-enhanced short (260bp) myosin light chain promoter (CMVenh/MLC260). Transaortic constriction (TAC) and sham operation was conducted 6 weeks later in 12 week old mice to induce pathological pressure overload. Organs were harvested 4 weeks after TAC at the age of 16 weeks and total RNA was used for microarray analysis. Three groups were compared: 1) sham-operated mice that were pretreated with AAV9 (CMVenh/MLC260)-Luc, 2) TAC-operated mice that were pretreated with AAV9 (CMVenh/MLC260)-Luc, 3) TAC-operated mice that were pre-treated with AAV9 (CMVenh/MLC260)-HDAC4-NT. Overall design: 3 male animals per group at an age of 8 weeks were included in the microarray analysis, treated with adenoassociated virus (AAV) containing a coding sequence for Luziferase or Histone Deacetylase 4 (HDAC4, aminoacids 1-201) under the control of the MLC-promoter. Both groups were then exposed to transaortic constriction. As a control to HDCA4 served AAV treatment with overepression of luziferase and sham-op as a control to TAC-surgery. Less...