Expression data for effect of p300 knockdown and Doxorubicin treatment in cardiac myocytes

Role of p300 in regulation of stress-response genes in heart is not clear. Treatment with anti-cancer drug Doxorubicin causes cardiotoxicity through generation of oxidative stress in cardiac myocytes. Loss of p300 enhances cell death and apoptosis in response to Doxorubicin. The objective of this study was to determine if expression of genes regulated by oxidative stress is dependent of presence of p300. Further we investigated if protective effect of p300 against Doxorubicin was due to gene expression effects of p300. We used microarray to compare the transcriptomes of cardiac myocytes transfected with anti-p300 or non-silencing siRNA beforebefore and after exposure to Doxorubicin. p300 was knocked down (p300kd) in primary culture of rat neonatal cardiac myocytes by using siRNA (Dharmacon). Cardiac myocytes transfected with non-siliencing siRNA (NS) were used as control. p300kd was confirmed by western blotting and real time PCR. Both NS and p300kd cells were treated for either 0 or 8 hrs with 1 micromolar Doxorubicin (Dox). Samples include p300kd and nonsilencing cells (0 and 8 hr Dox) from three different experiments.